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Stroke is very common in patients with sleep disordered breathing, especially in the elderly. We report the case of a 26-year-old man who had been referred to us with a sudden left side motor weakness of the body, headache, chronic fatigue, and witnessed sleep apneas. Intracerebral hemorrhage in the right external capsule and putamen was identified upon brain computed tomography. He had hypertension which had not been diagnosed previously. On polysomnography, apnea-hypopnea index was 73.0/h and arousal index was 74.7/h, indicating severe sleep apnea. Continuous positive airway pressure titration was conducted to determine the optimal pressure to alleviate the respiratory disturbances. Treatment with antihypertensive medication reduced blood pressure (BP) from 197/145 mm Hg to 130/80 mm Hg after 10 days of use. Co-treatment with the medication and auto-adjustable positive airway pressure additionally decreased BP to 110/60 mm Hg and normalized respiratory disturbances. In addition to BP, left hemiparesis, morning headache, daytime sleepiness, and chronic fatigue were all improved. Early treatment of OSA could help facilitate the rehabilitation of or recovery of weakness in such patients.

Background and Objective Many attempts have sought to devise an animal model of sleep fragmentation (SF) to understand the clinical effects of sleep loss, but no study has investigated the usefulness of the walking wheel method to interrupt sleep in rats. Methods Seven-week-old male Wistar rats were divided into a SF group and an exercise control (EC) group, with five rats in each. SF was achieved with a walking wheel using a 30 s on, 90 s off interval (total walking time 6 h/day). The EC group walked the same distance. Rat multiple sleep latency test was performed to measure sleepiness in rats. Sleep data were collected at baseline, and 4, 12, and 18 days after treatment. Percent (%) time spent awake and in non-rapid eye movement (NREM) and rapid eye movement (REM) sleep, NREM and wake bout number, NREM bout length, and mean sleep latency were analyzed. Results Numbers of NREM and wake bout were higher in the SF group, whereas the NREM bout length was smaller than in the baseline group. Unlike NREM, REM sleep (%) in the SF group was significantly lower than in the baseline and EC groups. Mean sleep latency was shortened in the SF group compared to the baseline and EC groups. EC did not differ significantly with respect to the amount of sleep time (%), bout number of NREM and wakefulness, NREM bout length, and mean sleep latency, compared to its own baseline. Conclusions Use of a walking wheel is an effective means of interrupting sleep in rats during a long-term period.

Background and Objective The association of sleep disturbance (SD) with cardiovascular disease is through its induction of autonomic dysregulation and inflammation, which also could be important pathophysiological mechanisms responsible for atrial fibrillation (AF). However, no study has fully elucidated the causal relationship between SD and AF. We investigated whether SD influences AF vulnerability in an in vivo rat model. Methods We divided 8-week-old Wister rats into 5 groups: 1) control, 2) 3-day SD, 3) 7-day SD, 4) 3-day sham SD, and 5) 7-day sham SD (n = 5 in each group), using the multiple platform method to create SD. We measured baseline heart rate, blood pressure (BP), and AF inducibility via burst atrial pacing (30 mA, 40 Hz, 30 seconds) by means of a transoesophageal electrode and used Sirius red staining to assess collagen deposition in the atriums. Results Baseline heart rate, diastolic BP and AF inducibility were significantly higher in the SD groups than in the control and sham condition groups (p < 0.05). However, there were no differences between the 3- and 7-day SD groups. Systolic BP and induced AF duration did not statistically differ among any of the experimental groups. The Sirius red staining showed no differences in collagen deposition among any of the experimental groups. Conclusions SD resulted in increase of AF inducibility in SD rats, suggesting that SD provides an atrial substrate for AF vulnerability, regardless of the disturbance period. However, induced AF duration showed no significant differences in SD rats.

Insomnia is a very common health problem affecting approximately 10-30% of the population in Western countries and approximately 23% of Korean adults.1-4 Medications based on chemical hypnotics, such as benzodiazepines, have the following adverse effects: diurnal ‘hangover’ effects, dependence, addiction, withdrawal symptoms, and subsequent drug-resistance.5 The demand for complementary and alternative medicines for treating insomnia is increasing, not only because patients wish to avoid the aforementioned adverse effects, but also because herbal/natural products are readily available and require no prescription from a doctor, in contrast to chemical drugs.6-8 Cynanchum wilfordii Hemsley (C. wilfordii)(Asclepiadaceae) is a perennial herb, whose roots have been widely used in Korea for treating insomnia, anxiety, anemia, senescence, and various geriatric diseases.9,10 However, despite its wide use in Korea, no objective studies evaluating its efficacy in treating or preventing insomnia exist. Therefore, in the present study, we evaluated C. wilfordii extract’s effects on the sleep-wake cycle in rats and compared it to valerian extract, an herbal product in widespread use for treating insomnia, to evaluate its possibilities as a natural hypnotic. Received: February 18, 2011 Revised: March 23, 2011 Accepted: April 1, 2011

Background and Objective Although Cynanchum wilfordii Hemsley (C. wilfordii) has been widely used for treating insomnia in Korea, there are no objective data on its sleep-enhancing effects. Methods We examined the effects of this extract on sleep latency, sleep parameters, and NREM delta activity in rats administered several different dosages (300 mg/kg, 1 g/kg or 3 g/kg, p.o.) and compared them to valerian extract which is a popular natural hypnotic. Results We found no significant shortening of sleep latency was observed with any dosage of either C. wilfordii extract or with valerian. NREM sleep increased significantly at C. wilfordii dosages of 300 mg/kg and 1 g/kg but not for 3 g/kg. Only the 1 g/kg dosage significantly decreased the amount of wakefulness. Neither any of the C. wilfordii dosages nor valerian extract produced any effect on REM sleep amount. Conclusions Therefore, C. wilfordii could be a useful natural hypnotic with a sleep-enhancing effect.

Background and Objective Simulated altitude as a model for hypoxia has shown inconsistent results in terms of impaired cognition. We hypothesized that preserved periods of stable sleep even under hypoxia could explain stable cognitive function. Delta spectral power on electroencephalography during stable sleep as well as high frequency coupling on the electrocardiogram-based spectrogram was adopted as measures of sleep quality. Methods Eleven healthy, non-smoking subjects (7 men, 27 ± 1.5 years) were exposed to 9 hours of continuous hypoxia for 13 consecutive nights. Polysomnography was done at baseline and during 3 time points, at night 3, 7, and 14. In each study, delta spectral power was obtained during stable N2 and N3 sleep. Stable sleep was defined when there was no significant fragmentation in electroencephalography and fluctuation in electromyography and cardiorespiratory signals. The time threshold was 2 or 5 continuous minutes for N2 and 2 minutes for N3. The amount of high frequency coupling for the sleep period on the electrocardiogram-based spectrogram was computed. Randomized block ANOVA was used with electroencephalography delta power and high frequency coupling as dependent variables with post hoc Tukey test. Results Delta spectral power during stable sleep was not significantly different across the entire hypoxic exposures (p = 0.98 for N2; p = 0.32 for N3). High frequency coupling was different between pre-exposure and mid-exposure (night 7; 52.5 ± 23.6% vs. 39.0 ± 16.7%, p = 0.02) but returned to the baseline level at the post-exposure (night 14; 45.4 ± 18.2%, p = 0.39). Conclusions Both preservation of the proportion of stable sleep and unchanged delta power during these periods may help explain maintained cognition in conditions of chronic nocturnal hypoxic exposures.

Gastroesophageal reflux disease (GERD) is a common condition that is characterized by the repeated overflow of stomach contents into the esophagus.1 In Western countries, the approximate prevalence of GERD ranges from 10% to 20% when defined by at least one heartburn and/ or acid regurgitation episode per week.2-4 In Asia, the prevalence rate is lower than those of Western countries (less than 5%).5,6 Individuals with GERD typically suffer from heartburn, acid regurgitation, and sometimes chest pain during day and night.1,7 GERD is associated with a variety of esophageal complications (e.g., esophagitis, stricture, and Barrett’s esophagus) and extra-esophageal syndromes (e.g., reflux cough, reflux laryngitis, asthma, and sleep apnea).1,7-9 Gastroesophageal reflux (GER) can occur both during sleep and while awake, but it is much less common during sleep.10 GER occurring during sleep may induce discomfort and frequent arousal. Therefore it could be an important cause of disrupted sleep. In this study, we present a case of frequent arousal following nocturnal dyspnea caused by GERD.

Treatment-emergent central sleep apnea has been referred to as ‘complex sleep apnea’, where apparently obstructive respiratory events convert to central apneas with application of positive airway pressure. Potential contributing factors may include increased propensity for arousals and positive airway pressure-induced reductions in CO2 which amplifies unstable ventilatory control. Here we demonstrate the dramatic beneficial effects of zolpidem and enhanced expiratory rebreathing space on complex sleep apnea, which helps to elude the mechanism of complex sleep apnea.