Nocturnal paralysis and tingling.
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The circadian, circasemidian and ultradian features of sleep-wake patterns in narcolepsy are reviewed with respect to the hypotheses that chronobiological disturbances might either be specific to the condition or contribute to its symptomatic profile. The position is taken that, while there are characteristic temporal features associated with the disorder, the chronobiological system is essentially intact, although quantitatively altered. It appears that the fundamental physiopathogenesis involves state boundary control mechanisms, which operate in state transitions, rather than chronobiological mechanisms affecting the timing of the manifestation of symptoms associated with the disease. We review our recent results from sleep-wake schedule studies designed to improve the maintenance of alertness in narcolepsy-cataplexy and report new analyses of subjective sleepiness data. The schedules employed were designed to take preexisting circadian, circasemidian and ultradian sleep-wake patterns of these patients into consideration.
Clinical features of cerebrovascular occlusive disease with the moyamoya network (group 1: twenty-nine children) and those without this network (group 2: nine children) are reported herein. Group 1 was characterized by female preponderance, recurrent and transient ischemic attacks, progression of mental deterioration, rebuild-up after hyperventilation on EEG and wide-spread lesions on CT scan. Group 2 had one or two attacks which led to a rather long-lasting hemiplegia but not to mental deterioration, rare rebuild-up findings on EEG and unilateral focal lesion on CT scan. Precipitating factors for ischemic attacks included deep breathing, changes in body temperature or sleep-waking transition were present in both groups. Etiology in some children was considered to be congenital.
STUDY OBJECTIVE: To examine the relationship between school grade level and sleep-phase preference in early adolescence. DESIGN: A school-based cross-sectional study using a Sleep Habit Questionnaire. SETTING: NA. PARTICIPANTS: One thousand five hundred and seventy-two students, grade 4 to grade 8, from 3 junior high schools and 3 elementary schools in Taipei were recruited using multistage sampling method. The response rates were 98.4% (1547) for participants and 95.9% (1509) for their parents. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Each student participant completed a Sleep Habit Questionnaire, including sleep schedules, the Morningness/Eveningness (M/E) scale, the Pubertal Developmental Scale, and the Sleepiness Scale. The morning (N = 367) and evening (N = 364) groups were operationally defined as participants with the top 25% and the bottom 25% of the M/E score, respectively. A mixed model was used in data analysis to address the cluster effects arising from the school-based study. We found that the M/E score decreased and the proportion of the evening type increased across grade 4 to grade 8. The evening type was associated with decreased nocturnal sleep and later bedtimes and rise times, as well as with increased daytime sleepiness and compensation for sleep on weekends. CONCLUSIONS: Our findings support the hypothesis that school grade level is significantly associated with the transition to evening type in early adolescence. We report that environmental factors may play a more important role than biologic factors, such as age, sex, and pubertal development, in the transition from morning type to evening type at early adolescence. Future longitudinal study is necessary to determine the trajectories of sleep-wake patterns in adolescents and their predictors.
The period of freerunning circadian rhythms is significantly shorter and the fraction of sleep is significantly larger in human females than in males, as long as the rhythms run internally synchronized. The sex difference in the period could be a property either of the whole circadian system or of only one of the oscillators in a multi-oscillator system. The sex difference in the sleep fraction could be a fixed property of the sleep-wake rhythm or could depend on interactions in the multi-oscillator system. To investigate these questions, a sample of 33 long-term experiments, in which the rhythms ran internally synchronized in one section and internally desynchronized in another section, were analyzed. The periods of rhythms in rectal temperature were different in females and males during internal synchronization, but became identical during internal desynchronization. In contrast, sex differences in sleep-wake periods were more pronounced when the rhythms were desynchronized than when they were internally synchronized. This result provides evidence that the sex difference in periodicity is a property only of the sleep-wake rhythm; the intrinsic periods of temperature rhythms are identical in females and males, whereas those of sleep-wake rhythms are distinctly shorter in females than in males. In the state of internal synchronization, the joint period is a compromise between the intrinsic periods of the rhythms involved, and therefore it shows a small but significant sex difference. Moreover, the transition from internally synchronized to desynchronized rhythms is combined with a highly significant reduction in the sleep fraction, which is considerably greater in females than in males. These results suggest that the occurrence of internal desynchronization strongly affects the sleep-wake rhythm, and that the influence of rhythm disorders is considerably greater in females than in males.
The objective of the present study was to evaluate the relationship between the sleep-wake behaviour and neurological impairments among mentally retarded people. The sleep-wake behaviour of 293 mentally retarded subjects living in a rehabilitation center was studied by a standardized observation protocol carried out by trained staff members. The protocol consisted of brief check-ups of the subjects' sleep-wake status at 20-min intervals for five randomly chosen 24-h periods during 4 months. From the raw data five sleep-wake behaviour variables were formed. The data concerning the subject characteristics (age, body mass index (BMI), gender, degree of mental retardation, presence of locomotor disability, that of epilepsy, blindness or deafness and the usage of psychotropic medications) were collected from the medical records. Two main findings emerged: (1) severe locomotor disability, blindness and active epilepsy were found to be independent predictors of increased daytime sleep and increased number of wake-sleep transitions and (2) the subjects with a combination of two or all three of these impairments had a significantly more fragmented and abnormally distributed sleep than those with none or milder forms of these impairments. Age, BMI, degree of mental retardation and the studied medications played a minor role in the sleep disturbances of the study population. Finally, deafness was not found to be associated with any of the measured sleep-wake variables.
Alterations in sleep organization were longitudinally studied in 6 new cases of fatal familial insomnia (FFI) by 24 h polygraphic recording. All patients showed an early reduction in sleep spindles and K complexes, and a drastic reduction in total sleep time and disruption of the cyclic sleep organization. Complete abolition of NREM sleep and persistence of only brief residual periods of REM sleep without atonia were features characteristic of the 3 patients with a short (less than 1 year) clinical course, and lacking in the 3 cases with a longer (more than 2 years) disease course. In the latter, sudden transitions from waking to NREM or REM sleep occurred, sometimes recurring periodically. Our findings confirm that impairment of sleep-wake regulation is a consistent distinctive feature of FFI.
Sleep disorders in amygdala-kindled cats differ according to the sleep or waking state in which seizures occur and the time lapse between seizures and polygraphic recordings. Twelve-hour polygraphic recordings were initiated at the following times: (i) before kindling (N = 8 cats); (ii) just after kindled convulsions during waking, slow-wave sleep (SWS), rapid-eye-movement sleep (REMS), or in transition from SWS to REMS (N = 8 cats per state), and (iii) 24 h after state-specific seizures (N = 8 cats per state). Rapid onset SWS and delayed REMS occurred in records started immediately after seizures in waking, SWS, or REMS; in contrast, seizures during transitions from SWS to REMS produced early onset REMS and SWS. Finally, records begun 24 h after seizures always revealed prolonged sleep onset and generalized sleep suppression regardless of the state in which seizures occurred. The timing of seizures and of polygraphic recordings may explain discrepancies in the literature on the type of sleep disorders seen in secondary generalized temporal lobe epilepsy.
Chronic exposure to mild unpredictable stress causes subsensitivity to rewards (anhedonia). These effects are reversible by chronic treatment with antidepressant drugs, and have been proposed as an animal model of depression. In the present study, sleep architecture, particularly the rapid eye movement (REM) component, was mapped in rats following exposure to chronic mild stress. The study used a unique large scale automated sleep system to record and analyze the sleep signals from 32 rats simultaneously. The effects of stress on sleep were maximal following 21 days of stress, at which time the stressed animals demonstrated decreases in active waking and deep sleep, and disruptions of REM sleep. The changes in REM sleep included increases in the duration of and transitions into REM sleep over the sleep part of the sleep-wake cycle, and most importantly, a reduced latency to the onset of the first REM period. These sleep abnormalities, and in particular the decrease in REM latency, are consistent with those reported in endogenous depression. The results provide further support for the validity of the chronic mild stress paradigm as an animal model to study the mechanisms underlying endogenous depression.
Biological circadian clocks oscillate with an approximately 24-hour period, are ubiquitous, and presumably confer a selective advantage by anticipating the transitions between day and night. The circadian rhythms of sleep, melatonin secretion and body core temperature are thought to be generated by the suprachiasmatic nucleus of the hypothalamus, the anatomic locus of the mammalian circadian clock. Autosomal semi-dominant mutations in rodents with fast or slow biological clocks (that is, short or long endogenous period lengths; tau) are associated with phase-advanced or delayed sleep-wake rhythms, respectively. These models predict the existence of familial human circadian rhythm variants but none of the human circadian rhythm disorders are known to have a familial tendency. Although a slight 'morning lark' tendency is common, individuals with a large and disabling sleep phase-advance are rare. This disorder, advanced sleep-phase syndrome, is characterized by very early sleep onset and offset; only two cases are reported in young adults. Here we describe three kindreds with a profound phase advance of the sleep-wake, melatonin and temperature rhythms associated with a very short tau. The trait segregates as an autosomal dominant with high penetrance. These kindreds represent a well-characterized familial circadian rhythm variant in humans and provide a unique opportunity for genetic analysis of human circadian physiology.
BACKGROUND: A hypnogram shows how sleep travels through its various stages in the course of a night. The sleep stage changes can be quantified to study sedative drug effects. METHODS: Hypnograms from 21 patients with primary insomnia were collected during a randomized, placebo-controlled crossover study of 20 mg temazepam. A separate daytime session was performed to determine the pharmacokinetics of 20 mg temazepam and its effect on saccadic eye movement and electroencephalogram. A first-order Markov model was developed to describe the probability of sleep stage changes as a function of time after drug intake and time after last sleep stage change. The influence of temazepam concentration on the probability to change sleep stage was incorporated into the model. RESULTS: Transitions between sleep stages were profoundly influenced by the time of the night and by the time since the last change of sleep stage. Temazepam reduced the time spent awake. This effect could be attributed to four mechanisms: (1) transition to "deeper" sleep was facilitated, (2) transition to "lighter" sleep was inhibited, (3) regardless of sleep stage, the transition to wake state was inhibited, and (4) return to sleep was facilitated. Daytime sensitivities to temazepam, measured with the surrogate markers saccadic peak velocity and electroencephalogram beta activity, each correlated with one of the transition probabilities influenced by temazepam. CONCLUSIONS: By the development of a Markov model for these non-ordered six categorical data, the effect of temazepam on the sleep-wake status could be interpreted in terms of known mechanisms for sleep generation and benzodiazepine pharmacology.
We studied the sleep-wake behavior of mentally retarded people from late winter to early summer at 60 degrees N. During this time the daylength increased 8 h 51 min. The data were collected by observing the sleep-wake status of 293 subjects at 20-min intervals for five randomized 24h periods (= recording days). The intervals during which the individual recording days of the same order (1st, 2nd, etc.) were carried out, were called recording periods. Consequently, there were five recording periods, each containing 293 individual recording days. Even though there was overlap among the recording periods, the median daylength from one period to another increased approximately by 100 min. In the initial statistical analysis, the number of wake-sleep transitions was found to differ significantly among the five recording periods (Friedman test, p < 0.001). The mean ranks in the Friedman test suggested that the number of wake-sleep transitions was highest during the 1st and lowest during the 5th recording period. In further statistical analyses using a program for mixed effects regression analysis (MIXOR 2.0) it was found that the increase in daylength during the study period was associated with a simultaneous decrease of approximately 0.5 wake-sleep transitions in the whole study population (p < 0.001). The decrease in the number of wake-sleep transitions was significant only in the subgroups of subjects with a daylength change of more than 350 min between the 1st and 5th recording days (Wilcoxon tests, p < 0.005). This suggests that after a marked prolongation of the natural photoperiod, the reduction in sleep episodes was more probable than after smaller changes in daylength. It is concluded that the sleep of mentally retarded people living in a rehabilitation center at a northern latitude is more fragmented in winter than in early summer and that the change is related probably to the simultaneous increase in the length of the natural photoperiod. The sleep quality of persons living in institutional settings might be improved by increasing the intensity and/or duration of daily artificial light exposure during the darker seasons.
STUDY OBJECTIVES: Because sleep and wakefulness differ from each other by the amount of body movement, it has been claimed that the two states can be accurately distinguished by wrist actigraphy. Our objective was to test this claim in lengthy polysomnographic (psg) and actigraphic (acf) samples that included night and day components. DESIGN: Fourteen healthy young (21-35 years) and old (70-72 years) men and women lived in a laboratory without temporal cues for 7 days. Each subject continuously wore sleep-recording electrodes as well as 2 wrist-movement recorders. Act measurements were converted to predictions of sleep and wakefulness by simple-threshold and multiple-regression methods. Psg served as the gold standard for calculation of predictive values (PV, the probability that an act prediction is correct by psg criteria). SETTING: N/A. PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The 7-day act recordings showed clear circadian cycles of high and low activity that respectively corresponded to subjective days, when subjects were wakeful, and subjective nights when they slept. Lower act levels corresponded to deeper states of psg sleep. Logistic regression on a 20-minute moving average of act gave the highest overall PV's. Nevertheless, the mean PV for sleep (PVS) was only 62.2% in complete, day + night samples. PVS was 86.6% in night samples. Act successfully predicted wakefulness during subjective nights (PVW = 89.6) and accurately measured circadian period length and the extent of sleep-wake consolidation, but it overestimated sleep rate and sleep efficiency. Act systematically decreased before sleep onset and increased before awakening, but reliable transitions among joint psg/act states (the Markov-1 property) were not demonstrated. CONCLUSIONS: Low PV's and overestimation of sleep currently disqualify actigraphy as an accurate sleep-wake indicator. Actigraphy may, however, by useful for measuring circadian period and sleep-wake consolidation and has face validity as a measure of rest/activity.
This review article: (1) describes the circadian distribution of ictal and interictal events; (2) differentiates transitional arousal, non-rapid eye movement and rapid eye movement sleep components and their substrates; (3) suggests the means by which the neural generators of these seizure-prone vs. seizure-resistant sleep and arousal states modulate the timing of different seizure manifestations; (4) considers clinical and mechanistic findings for the reciprocal effects of seizures and antiepileptic drugs upon the sleep-wake cycle; and (5) assesses clinical and basic mechanisms of sleep deprivation effects upon seizures.
Amygdala-kindled kittens exhibit frequent epileptiform EEG transients, often in conjunction with phasic arousal events of sleep [k-complexes, pontogeniculo-occipital (PGO) waves, and/or sleep spindles]. In this study, paroxysmal microarousals occurred throughout the sleep-wake cycle after kindling, but were most frequent during seizure-prone states of slow-wave sleep (SWS) and the transition into rapid-eye-movement sleep (REM). Their incidence correlated with interictal sleep fragmentation as well as onset of spontaneous convulsions. Results could reflect transsynaptic kindling effects on brainstem and forebrain arousal mechanisms with which amygdala is reciprocally connected. Increased discharge rates of neural generators for normal EEG and behavioral arousal could disrupt sleep at some times and recruit epileptic neurons in the kindled focus to precipitate seizures at others. Alternatively, epileptiform EEG paroxysms were accompanied by subtle behavioral stereotypes (a head nod, limb elevation, eye twitch, lip smack, or a combination of these). Behavioral correlates were elements of partial kindled seizures, suggesting that paroxysmal microarousals may be subclinical seizures. Whether or not the microarousals are true seizures, our findings may link ictal onset and interictal sleep disorders to a subclinical paroxysmal arousal disorder and suggest a common epileptic mechanism.
The effects of immediate-release melatonin on circadian rest-activity profiles, cognition, and mood were investigated in ten elderly individuals with self-reported sleep-wake disturbances. Melatonin (6 mg), administered 2 hr before habitual bedtime, enhanced the rest-activity rhythm and improved sleep quality as observed in a reduction in sleep onset latency and in the number of transitions from sleep to wakefulness. However, total sleep time was not significantly increased nor was wake within sleep significantly reduced. The ability to remember previously learned items improved along with a significant reduction in depressed moods. No side effects or contraindications were reported by any of our participants during the 10 day trials. These data suggest that melatonin can safely improve some aspects of sleep, memory, and mood in the elderly in short-term use.