Rapid eye movement sleep cycle, clock time and sleep onset.

The phase of the REM sleep rhythm was studied in 10 normal subjects each of whom was sleep studied for 4 consecutive nights. For analysis, each night of sleep was aligned according to clock time and each minute was scored as REM or non-REM. With these data, REM probability was found as a function of clock time. Fractional harmonic analysis indicates a 90 min periodicity. The REM probability curve shows peaks occurring at 1:30 a.m., 3:15 a.m., 4:30 a.m., 5:45 a.m. and 7:00 a.m. Statistical measures comparing the time of REM sleep across subjects suggests that subjects tend to have REM sleep at the same time of the night as each other. The influence of elapsed time after sleep onset on REM sleep is also reestablished. Results indicate that the time of REM sleep is determined by both clock time and time of sleep onset, suggesting two clocks, one sleep dependent and the other related to the basic rest activity cycle (BRAC), which are responsible for driving REM sleep. Furthermore, the similarity of REM times across subjects indicates the possible existence of an extra-personae REM driving force linked to clock time and possibly the BRAC.     

Effect of HLA type on age at onset in schizophrenic disorders

In a sample of 229 patients affected by schizophrenic disorders according to DSM-III, the authors tested the effect of the HLA type, sex and severity of the disease with respect to the distribution of age at onset. All the three factors reached, independently, a statistically significant value: that is, HLA A1 positive males affected by the severe form of the illness show the earliest breakdown of the disease. This finding partially confirms previous results, and particularly the importance of the HLA influence is discussed.     

Effect of age at onset on progression and mortality in Parkinson's disease

We examined longitudinal disability scores in 54 patients with Parkinson's disease followed for 6 years at UCLA. We sorted data into 3 groups based on age at onset of symptoms: group A, onset under 50 years; group B, 50 to 59 years; group C, 60 years or older. There were no significant differences between groups initially. All 3 groups improved dramatically when levodopa was given, but group A showed significantly less disability in years 4, 5, and 6 than did group C. The groups did not differ with respect to side effects. To determine if age at onset affected mortality, we sorted records from 4 geographically diverse centers into the same 3 groups. Results on 359 patients followed for 3,314 person-years, covering a period of 17 years after onset of symptoms, showed that group A had the most favorable observed-to-expected mortality ratio, 1.82, compared with 2.17 and 2.20 for groups B and C respectively, but the difference was not statistically significant. Results from the disability analyses indicate that patients with onset of Parkinson's disease under 50 years of age may have a more favorable prognosis than those whose symptoms begin in later years.     

Effect of age at onset on frequency of depression in Parkinson's disease.

In a consecutive series of 169 outpatients with Parkinson's disease the frequency of depression was compared in two groups: those who developed Parkinson's disease before the age of 50, and those who developed the disease after 50. Major depression was found in 36% of patients with early onset and in 16% of patients with late onset Parkinson's disease. This significant difference disappeared when both groups were matched for duration of Parkinson's disease. A stepwise regression analysis in both the early onset and the late onset Parkinson's disease showed a significant correlation only between depression scores and the impairment scores of activities of daily living.     

Effect of climatic temperature on the age of onset of Huntington's chorea

The age of 1,403 subjects at onset of Huntington's chorea were drawn from the literature and related to the mean annual, January, and July temperatures of their place of residence. When the data were converted into mean annual, winter, and summer isotherms covering a range of 10° F (5·6° C), there was a statistically significant decrease in age of onset as the temperature increased. Over the ranges studied, winter temperatures exerted a stronger effect than summer temperatures. To reduce interference by ethnic factors, the analysis was repeated on North American subjects with similar results. It is suggested that repeated infections may provoke chorea and that the observed lowering of the age of onset is associated with increased susceptibility to infection on passing from cold to warm climates.     

Effect of age at onset on the course of major depressive disorder

OBJECTIVE: This report assesses whether age at onset defines a specific subgroup of major depressive disorder in 4,041 participants who entered the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study. METHOD: The study enrolled outpatients 18-75 years of age with nonpsychotic major depressive disorder from both primary care and psychiatric care practices. At study entry, participants estimated the age at which they experienced the onset of their first major depressive episode. This report divides the population into five age-at-onset groups: childhood onset (ages <12), adolescent onset (ages 12-17), early adult onset (ages 18-44), middle adult onset (ages 45-59), and late adult onset (ages > or =60). RESULTS: No group clearly stood out as distinct from the others. Rather, the authors observed an apparent gradient, with earlier ages at onset associated with never being married, more impaired social and occupational function, poorer quality of life, greater medical and psychiatric comorbidity, a more negative view of life and the self, more lifetime depressive episodes and suicide attempts, and greater symptom severity and suicidal ideation in the index episode compared to those with later ages at onset of major depressive disorder. CONCLUSIONS: Although age at onset does not define distinct depressive subgroups, earlier onset is associated with multiple indicators of greater illness burden across a wide range of indicators. Age of onset was not associated with a difference in treatment response to the initial trial of citalopram.     

Effect of ropinirole on sleep onset: a randomized, placebo-controlled study in healthy volunteers

Somnolence and "sleep attacks" have been reported as an adverse effect of several antiparkinsonian drugs. The authors document, in a placebo-controlled, randomized, double-blind, crossover study performed in 20 healthy volunteers, using the Multiple System Latency Test (MSLT) as primary outcome, that ropinirole reduces time to sleep onset in humans. Ropinirole therapy was not associated with daytime episodes of rapid eyes movement (REM) sleep.     

遗传因素和铁蛋白水平与不宁腿综合征发病年龄的关系

目的探讨家族遗传因素和血清铁蛋白水平与早发不宁腿综合征和晚发不宁腿综合征的关系。方法对35例原发性不宁腿综合征病例按照国际惯例分为早发不宁腿综合征组(21例)和晚发不宁腿综合征组(14例),分别统计家族史有无及血清铁蛋白水平,并进行统计学分析。结果早发不宁腿综合征组家族史阳性率(57.1%)高于晚发不宁腿综合征组(14.3%),而晚发不宁腿综合征组血清铁蛋白水平(67.66±28.14ng/ml)较早发不宁腿综合征组(104.52±54.02ng/ml)低,差异均有统计学意义(P<0.05)。结论遗传因素对早发不宁腿综合征的影响大于晚发不宁腿综合征,而血清铁蛋白的降低对晚发不宁腿综合征的影响大于早发不宁腿综合征。     

Effects of L-tryptophan on sleep onset insomniacs.

Eighteen female subjects with demonstrated laboratory sleep onset latency greater than 20 minutes for two nights participated in this double blind study of the effectiveness of l-tryptophan as a hypnotic. Standard sleep recordings were made on 10 nights over a 3 month period with lights out occurring 20 minutes after drug administration (placebo, 1 gm. l-tryptophan, 3 gms. l-tryptophan). Neither dose of l-tryptophan differed from placebo as to the amount of REM, SWS or wakefulness, but 3 gms. significantly reduced sleep onset latency on some of the nights. Those subjects with latencies longer than 40 mins. had the greatest reduction in latency with 3 gms. and also evidenced high levels of anxiety on the Taylor Manifest Anxiety Scale initially. Subjects with latency between 20 and 40 minutes appeared to receive the longest lasting hypnotic effect from the higher dose. Adaptation to the sleep lab took place across the entire 10 nights of the study. Therefore, valid comparisons between treatments in a sleep study extending over a number of nights should be made between temporally adjacent samples.     

Sleep onset and first cycle of sleep in human subjects: change with time of day.

The first cycle of sleep was studied in different situations: normal night sleep, naps, diurnal sleep after night shifts (3 x 8 shift workers). Results show two types of first cycle: some started with SWS (normal cycles), others with REM (sleep onset REM periods: SOREMPs). (1) Normal cycles: the length of SWS in the first cycle was positively correlated with prior wakefulness; conversely, the latency of SWS decreased as prior wakefulness increased; the decrease was due to the decrease in the length of the previous stage II or of the sleep onset latency (SOL). Length of sleep onset (SO) showed only few variations. The structure of the first cycle of shift workers' sleep probably reflects an important sleep loss. (2) SOREMPs occcurred during diurnal sleep. Some hypotheses about these cycles are discussed including REM 'pressures' (circadian, sleep loss) and inter-individual variations.     

Monitoring sleep hours using a sleep diary and errors in rotating shiftworkers

The sleep hours of male workers on rotating shift schedules were measured using a sleep diary. The mean age of workers was 40.3 years. Work shifts were rotated on a weekly basis and fell into three periods: morning, evening, and night. One working week consisted of 5 days. Errors that occurred during the work were also evaluated. A significant difference in the mean length of sleep was observed for each of the three shifts. Compared with the morning shift, the length of sleep for workers working evening and night shifts were significantly longer. The error of workers was not recognized in three rotating shift schedules in the survey period. Rotating shiftwork affects the amount of sleep, but not the event of error.     

Effects of bright light pre-exposure on sleep onset process

This study investigated the effects on the sleep onset process of enhanced cerebral cortex activity caused by bright light pre-exposure. Seven healthy young adults were exposed for 40 min before sleep onset, 2500 lx of bright light and 10 lx of dim light. Other factors that affect sleep onset (e.g. circadian phase) were experimentally controlled. Five stages of hypnagogic electroencephalogram (EEG) were scored. The latency of each EEG stage was longer at bright light than at dim light conditions, suggesting that activation of brain activity by bright light pre-exposure strongly regulates the sleep onset process.