SLEEP

Szeto, Hazel, H.;Zhu, Yuan, Shan;Amione,, John;Clare,, Sonia

doi: 10.1093/sleep/11.2.121pmid: 3381053

Summary: We have previously shown that acute exposure to low-dose morphine stimulates arousal and breathing movements in the fetal lamb. We now report on the effects of subacute low-dose morphine exposure on the regulation of fetal sleep-wake behavior and breathing patterns. Morphine was infused to 11 fetal lambs (121–129 days gestation) at a constant rate of 400 μg/h for 7 days via a mini osmotic pump implanted subcutaneously in the maternal flank and connected directly to an indwelling catheter in the fetal vena cava. On day 1, morphine resulted in a state of arousal in all fetuses, with loss of quiet sleep and rapid eye movement (REM) sleep. This response was greatly reduced by day 2 and was insignificant by day 3, despite continuous drug exposure. There was no decrease in plasma morphine levels. Two fetuses died during morphine exposure. Upon removal of the pump, all fetuses exhibited disturbances in their sleep cycles within 1–3 h, with an increase in arousal time and loss of REM sleep. The duration of the arousal and quiet sleep episodes was also greatly reduced. Such disturbances were noted for 3–4 days after termination of morphine infusion. Four fetuses were delivered prematurely (131–136 days) during this period. These results demonstrate the rapid onset of tolerance to low-dose morphine exposure in the fetus and the development of physical dependence, as manifested by a mild abstinence syndrome characterized by sleep-wake disturbances. Morphine, Sleep, Fetus, Tolerance and dependence, Opiates This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Salinsky,, M.;Goins,, S.;Sutula,, T.;Roscoe,, D.;Weber,, S.

doi: 10.1093/sleep/11.2.131pmid: N/A

Abstract Summary Color Density Spectral Array (CDSA) is a new technique that uses the fast Fourier transform and color graphics to provide a display of frequency , power, and time. CDSA sleep records provide an overview of sleep architecture as well as quantitive EEG data. To validate this technique, overnight sleep records from five patients were independently staged from polygraph recordings and overnight CDSA records. Observed agreement between the two techniques was 85–92% for approximately 1,100 epochs per night. Sleep, Color density spectral array This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Ogilvie, Robert, D.;Wilkinson, Robert, T.

doi: 10.1093/sleep/11.2.139pmid: 3381055

Summary: Faint tones were presented at intervals (average 16 s) throughout a night's sleep; whenever they heard them, subjects pressed a palm-mounted button to switch them off. At the same time, electroencephalogram (EEG) was recorded. Button-press responses occurred in all EEG stages of sleep except Stage 4, although there was only one behavioral response (BR) in Stage 3 and one in REM. The mean probability of response (PR)/Stage was Stage 1 = 0.235, Stage 2 = 0.016, Stage 3 = 0.001, Stage 4 = 0.000, Stage REM = 0.0004. Also, responses sometimes failed to occur in EEG Stage wake (PR = 0.94), particularly near sleep onset. If the criterion for wakefulness is cognitive response to external stimulation, only in EEG Stages 3, 4, and REM can accurate distinctions between sleep and wakefulness be made. If EEG is the criterion, then the data suggest that cognitive response is possible during Stages 1 and 2 “sleep.” The concept of a sleep onset period (SOP), characterized by lengthening response times and intermittent response failure (thereby reflecting neither true sleep or wakefulness), may provide a useful resolution of this definitional dilemma. Sleep, Sleep onset, Sleep onset period, Sleep/wakefulness definition This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Maselli, Ricardo, A.;Rosenberg, Richard, S.;Spire,, Jean-Paul

doi: 10.1093/sleep/11.2.156pmid: N/A

Abstract Summary Twelve patients, aged 19 to 29 years, presented with episodic nocturnal wanderings characterized by stereotyped frequent attacks of screaming, ambulation, and complex automatisms during sleep. The attacks ranged in frequency from two or three per year to several per night and were often associated with semi-purposeful violent and even life-threatening behavior. None of the patients had a history of seizures; three had a history of prior parasomnias and four had family members with a history of parasomnia. Polysomnographic and daytime electroencephalographic (EEG) investigations showed potentially epileptiform activity in four patients. Recorded episodes were not accompanied by ictal EEG activity. Anticonvulsant medication reduced or eliminated the attacks in all of the nine treated patients. The pathophysiology of the disorder is uncertain. Nocturnal wanderings, Parasomnias, Epilepsy This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Shouse, Margaret, N.

doi: 10.1093/sleep/11.2.162pmid: 3381057

Summary: The timing of amygdala kindled and penicillin seizures was studied throughout the sleep-wake cycle in eight cats following near total sleep deprivation and a control procedure that did not affect sleep time. Sleep loss was induced by 24-h exposure to a modified “flower pot” procedure employing a small pedestal. The control procedure consisted of 24-h exposure to a larger pedestal. Sleep loss increased susceptibility to generalized kindled and penicillin seizures during all waking and sleep states but did not alter temporal patterns of seizure susceptibility. Both before and after sleep loss, kindled cats showed maximal seizure susceptibility, indexed by lowest seizure thresholds, during slow wave sleep (SWS) and transitions from SWS to REM sleep (REMS). The spike-wave discharges and motor seizures of systemic penicillin epilepsy were always most frequent during SWS and during drowsiness after awakening. Both models were invariably most resistant to seizures during stable REMS. To explain sleep- and sleep loss-activated seizures, we summarized previous work suggesting that sleep abnormalities dictate the timing of seizures and are exacerbated by sleep loss. Abnormal behavioral arousals and pathological somatomotor system excitability occur in both models and are particularly pronounced during seizure-prone intervals. Sleep loss may magnify somatomotor system hyperexcitability patterns in all states, thus allowing abnormal motor arousals and seizures to intrude during seizure-prone and seizure-resistant sleep and waking states. Slow wave sleep, REM sleep, Penicillin epilepsy, Amygdala kindling, Sleep deprivation This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Ware, J., Catesby;Rugh, John, D.

doi: 10.1093/sleep/11.2.172pmid: 3381058

Summary: Despite apparent similar amounts of bruxism, two groups that had been evaluated polysomnographically differed dramatically in symptomatology. Patients with severe symptoms were referred to as the destructive bruxism group and were compared with (a) a group with sleep disturbance complaints who had bruxism and (b) a group of insomniac depressed patients chosen without regard to bruxism. It was hypothesized that not only the presence of bruxism during sleep but its pattern and sleep stage relationship were factors affecting clinical symptoms. The results indicated that the sleep stage relationship was an important factor. Patients with severe symptoms attributed to nocturnal bruxism were likely to have more bruxism in REM sleep than the other groups. These results if replicated prospectively would help explain some of the discrepancies in the literature concerning sleep stage relationship of bruxism, as well as help explain differences in symptomatology of bruxism patients. Sleep, Bruxism, Depression, Temporomandibular joint pain This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Ware, J., Catesby;Blumoff,, Ronald;Pittard, Joe, Tom

doi: 10.1093/sleep/11.2.182pmid: 2898166

Summary: Two patients complaining of insomnia had sleep-related periodic leg movements (nocturnal myoclonus) on polysomnographic evaluation. Both also complained of cold feet and had abnormal peripheral pulse examinations. Treatment with phenoxybenzamine, a-adrenergic blocker, normalized the peripheral pulse responses, reduced the complaint of insomnia, and reduced the sleep related leg movements but resulted in only mild sleep improvements. Peripheral pulse examinations of ten other patients with sleep-related periodic leg movements revealed abnormal responses in four. From these and other results, it is hypothesized that the sympathetic nervous system may mediate the periodicity of sleep related periodic leg movements. Nocturnal myoclonus, Sleep, Sympathetic nervous system, Sleep-related periodic leg movements, Peripheral vasoconstriction This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Askenasy, J. J., M.

doi: 10.1093/sleep/11.2.187pmid: 3381059

Summary: The present study is the first to prove the presence of hiccup during sleep polygraphically. Hiccup (Hc) penetrates all sleep stages; in REM sleep, it becomes randomized. The amplitude and frequency of sleep Hc have stage-dependent characteristics, and a linear regression appears with every sleep cycle. Sleep Hc may alternate, but does not coexist with, periodic leg movements. Related to inspiration, sleep Hc presents a right deviation when compared with wake Hc. The sleep pattern in persistent sleep Hc is disturbed in a nonspecific manner. Sleep Hc is not associated with sleep apnea. Sleep synchronizes the breathing rate with the hiccupping rate. During light sleep, the Hc rate exceeds the breathing rate, whereas during deep sleep, the breathing rate exceeds the Hc rate. Sleep hiccup, Wake-sleep hiccup, Wake hiccup, REM random hiccup, Hiccup rate This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Libert, J., P.;, Di Nisi, J.;Fukuda,, H.;Muzet,, A.;Ehrhart,, J.;Amoros,, C.

doi: 10.1093/sleep/11.2.195pmid: 3381060

Summary: Six young men were exposed to a thermoneutral environment of air temperature (Ta) 20°C for 5 days and nights followed by an acclimation period of 5 days and nights at Ta 35°C and 2 recovery days and nights at Ta 20°e. Electrophysiological measures of sleep, esophageal temperature, and mean skin temperature were continuously monitored. The total nocturnal body weight loss was measured by a sensitive platform scale. Compared with the 5 nights of the baseline period at 20°C, sleep patterns showed disturbances at 35°C. Total sleep time was significantly reduced, while the amount of wakefulness increased. The subjects exhibited fragmented sleep patterns. The mean duration of REM episodes was shorter at 35°C than at 20°C of Ta, while the REM cycle length shortened. In the acclimation period, there was no change in sleep pattern from night to night, despite adaptative adjustments of the thermoregulatory response. The protective mechanisms of deep body temperature occurring with heat adaptation did not interact with sleep processes. Upon return to baseline condition, a recovery effect was observed on a number of sleep parameters which were not significantly affected by the preceding exposure to prolonged heat. This would suggest that during exposure to dry heat, the demand for sleep could overcome that of other regulatory functions that are temperature-dependent. Therefore, a complete analysis of the effect of heat on sleep parameters can be assessed only if heat exposure is compared with both baseline and recovery periods. Sleep disturbance, Adaptation to heat This content is only available as a PDF. © 1988 Association of Professional Sleep Societies

Bunnell, David, E.;Agnew, James, A.;Horvath, Steven, M.;Jopson,, Linda;Wills,, Marsha

doi: 10.1093/sleep/11.2.210pmid: 3381061

Summary: Previous studies have found enhanced delta sleep following body heating. This study assessed the influence of body heating as a function of its proximity to sleep. Electroencephalogram (EEG) sleep patterns were compared following body heating (l h immersion in water at 41°C) at each of four times of day: morning (MO), afternoon (AF), early evening (EE), and late evening (LE), ending just prior to sleep. A delta filter/integrator system provided objective measures of delta content. Relative to baseline nights, wholenight delta sleep was increased by the two evening heating sessions only, particularly LE heating. Following LE, the increased delta occurred primarily in the first sleep cycle, whereas EE heating elicited increased delta distributed across the later sleep cycles (cycles 2–4). Effects on manually staged indices of slow wave sleep (SWS) were confined to increases in Stage 4 in the first sleep cycle following LE heating. Heating just prior to sleep also resulted in a substantial reduction in the duration of the first rapid eye movement sleep period. Sleep onset time was reduced by heating, particularly EE heating. The results indicate that body heating induces temporary changes that affect sleep propensity and both the quantity and temporal distribution of delta activity in the sleep EEG. Slow-wave sleep, Delta sleep, Temperature and sleep, Body heating and sleep, Sleep regulation This content is only available as a PDF. © 1988 Association of Professional Sleep Societies