The 10-year risk of verified motor vehicle crashes in relation to physiologic sleepiness.

STUDY OBJECTIVES: The purpose of this study was to determine the risk of DMV documented crashes as a function of physiological sleepiness in a population-based sample. DESIGN: 24-hour laboratory assessment (nocturnal polysomnogram and daytime MSLT) and 10-year crash rate based on DMV obtained accident records. PARTICIPANTS: 618 individuals (mean age = 41.6 +/- 12.8; 48.5% male) were recruited from the general population of southeastern Michigan using random-digit dialing techniques. RESULTS: Subjects were divided into 3 groups based on their average MSLT latency (in minutes) as follows: excessively sleepy, 0.0 to < or = 5.0 (n = 69); moderately sleepy, 5.0 to < or = 10.0 (n = 204); and alert, > 10 (n = 345). Main outcome measures were DMV data on accidents from 1995-2005. Rates for all accidents in the 3 MSLT groups were: excessively sleepy = 59.4%, moderately sleepy = 52.5%, alert = 47.3%. Excessively sleepy subjects were at significantly greater risk of an accident over the 10-year period compared to alert subjects. A similar relation was observed when we limited the database to those accident victims with severe injury (excessively sleepy = 4.3%, moderately sleepy = 0.5%, alert = 0.6%; P = 0.028). When the victim was the only occupant of the car, subjects in the lowest MSLT group (highest sleepiness) had the greatest crash rate compared with alert individuals (excessively sleepy = 52.2%, moderately sleepy = 42.2%, alert = 37.4%; P = 0.022). INTERVENTIONS: N/A. CONCLUSIONS: These data demonstrate that the MSLT, a physiological measure of sleepiness, is predictive of an increased risk of DMV documented automotive crashes in the general population.

Periodic limb movements during sleep: population prevalence, clinical correlates, and racial differences.

STUDY OBJECTIVE: There is growing interest in the study of periodic limb movements during sleep and their potential clinical correlates. The aim of the present analysis is to address the lack of population-based studies using polysomnographic (PSG) measures to determine the prevalence of period limb movements during sleep in specific racial groups as well as the general population. SETTINGS AND PARTICIPANTS: A community-based sample of 592 participants drawn from the general population of tricounty Detroit (mean age = 41.9 +/- 12.6 years; 52.9% F; 31.5% African American). All individuals were assessed using objective and subjective measures in the sleep laboratory. MEASUREMENTS: Participants were evaluated during a 24-h laboratory assessment, including a polysomnogram and multiple sleep latency test. Periodic leg movements were scored using standard criteria. Reports of sleep disturbance and daytime sleepiness were also assessed using standardized measures including the Global Sleep Assessment Questionnaire (GSAQ) and the Epworth Sleepiness Scale (ESS). RESULTS: The overall prevalence of periodic limb movements during sleep (PLMSI >15) was 7.6%. African Americans had a lower prevalence of PLMSI >15 than Caucasians (4.3% vs. 9.3%; chi2= 4.5, P < 0.05). Regardless of race, symptoms of insomnia were significantly higher in individuals with PLMSI >15 than in those with PLMSI < or =15 (45% vs. 25%; chi2= 6.84, P < 0.01). CONCLUSION: This is the first study to determine the prevalence of PLMS in a population-based sample using standardized objective criteria. A key finding of the present study is that racial differences in this PSG parameter do exist, with African Americans being less likely to have elevated PLMS.

Vulnerability to insomnia: the role of familial aggregation.

BACKGROUND: The goal of this study was to determine the degree of familial aggregation in vulnerability to stress-related sleep disturbance among siblings. One approach to investigating a potential "familial" predisposition to sleep disturbance is to examine the relationship between siblings on a standard measure of vulnerability to stress-related sleep disturbance. DESIGN: Cross-sectional data on insomnia, vulnerability to stress-related sleep disturbance, sleepiness, habitual sleep, and additional demographic variables was collected separately from pairs of biological siblings. Data were collected during a 15-20min phone assessment. PARTICIPANTS: Interviews on a total of 62 individuals (31 sibling pairs) were completed. A total of 8 individuals and their respective siblings were excluded after meeting conservative criteria for Diagnostic and Statistical Manual of Mental Disorders, Fourth edition (DSM-IV)-based insomnia. The mean age of the sample was 51.1+/-12.1 years (range 18-70) and habitual nightly total sleep time averaged 6.91+/-1.42h/night. RESULTS: Individuals completed the Ford Insomnia Response to Stress Test (FIRST), a standardized measure of individual vulnerability to stress-induced sleep disturbance. The intraclass correlation coefficient (ICC) was r =0.61, df=23, p =0.001 for the relationship between siblings in FIRST scores. This indicated that 37.2% of the variance in vulnerability to stress-related sleep disturbance can be accounted for by familial aggregation. This relationship remained after controlling for potential confounds including age, gender, shift schedule, and psychiatric history. CONCLUSIONS: Our data support the notion that vulnerability to stress-related sleep disturbance has a strong familial aggregation. Additional studies are needed to determine the genetic or environmental origins of this relationship and its underlying biological substrates.

Sleep hygiene practices in a population-based sample of insomniacs.

STUDY OBJECTIVES: The present study was designed to assess selected aspects of sleep hygiene from a population-based sample of individuals with insomnia compared to age- and sex-matched controls. DESIGN: A random-sample phone survey of 258 individuals meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-based criteria for insomnia was compared to age- and sex-matched normal sleepers on specific measures of sleep hygiene. Sleep hygiene practices measured included cigarette smoking, smoking near bedtime, alcohol use, caffeine use, napping, time in bed, and reported likelihood of sleeping in on weekends. SETTING: Detroit tricounty population. PARTICIPANTS: 258 individuals 18 to 65 years old with insomnia and 258 age- and sex-matched controls. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Insomniacs reported poorer sleep hygiene, as evidenced by an increase in prevalence of smoking close to bedtime and increased use of alcohol. They also reported more naps per week and sleeping in on days not worked. Caffeine use did not differ between groups. Time in bed was also comparable between insomniacs and controls. CONCLUSION: Insomniacs do engage in specific poor sleep hygiene practices, such as smoking and drinking alcohol just before bedtime. These particular aspects of sleep hygiene may be important components that exacerbate or perpetuate insomnia.

Vulnerability to stress-related sleep disturbance and hyperarousal.

STUDY OBJECTIVES: To determine the presence of a hypothesized trait vulnerability to sleep disturbance and hyperarousal. DESIGN: Polysomnographic assessment of sleep in response to stress during a first night in the laboratory and subsequent physiologic arousal. PARTICIPANTS: One hundred and four individuals (46% men, mean age 40.4 +/- 12.9 years) drawn from a population-based sample. INTERVENTIONS: Individuals were exposed to a first night in the laboratory. MEASUREMENTS AND RESULTS: Participants completed a Likert-scale questionnaire, consisting of 27 items, that assesses sleep disturbance in response to commonly experienced stressful situations. Factor analytic techniques identified a single 9-item factor that was representative of the construct of "stress-related" vulnerability to sleep disturbance. Reliability of the resulting 9-item scale was high (Cronbach's alpha = .83). Individuals with higher scores on this scale, the Ford Insomnia Response to Stress Test (FIRST; median split), had a lower sleep efficiency (P = .001), as well as an increased latency to stage 1 sleep (P = .001) and persistent sleep (P = .002) on the first night of nocturnal polysomnography. Moreover, these high-scoring individuals showed increased arousal as evidenced by an elevated sleep latency on the Multiple Sleep Latency Test compared to individuals with low FIRST scores. Importantly, after controlling for current and past insomnia, the differences between individuals scoring high and low on the FIRST in terms of nocturnal sleep and daytime arousal remained significant. Other stages of sleep (stage 2, slow-wave, and rapid eye movement sleep) were not different between the groups. CONCLUSIONS: These results showing a relationship between FIRST scores and nocturnal polysomnography and Multiple Sleep Latency Test scores have 3 potential implications: (1) the data demonstrate a characteristic that relates to vulnerability to stress-related sleep disturbance as manifested by a first night in the laboratory; (2) the elevated latencies on the Multiple Sleep Latency Test in these individuals, despite significantly disturbed sleep, support the notion of physiologic hyperarousal in these individuals and suggests they may be predisposed to developing chronic primary insomnia; and (3) the vulnerability identified may underlie vulnerability to transient sleep disturbance associated with other sleep-disruptive factors.

Caffeine reversal of ethanol effects on the multiple sleep latency test, memory, and psychomotor performance.

Caffeine has been shown to reverse some of the performance-impairing effects of ethanol. However, it is not known whether this antagonistic effect of caffeine is mediated by a reduction in sleepiness. The present study assessed physiological alertness/sleepiness, memory, and psychomotor performance following the administration of placebo, ethanol, and caffeine+ethanol combinations. A total of 13 healthy individuals (21-35 years old) underwent four conditions presented in a Latin Square Design: placebo-placebo, ethanol (0.5 g/kg)-placebo, ethanol (0.5 g/kg)-caffeine 150 mg, and ethanol (0.5 g/kg)-caffeine 300-mg. The Multiple Sleep Latency Test (MSLT), psychomotor performance battery, memory test, and mood/sleepiness questionnaires were administered following each condition. The peak breadth ethanol concentration (BrEC) was 0.043+/-0.0197% and did not differ among the three caffeine treatments. As expected, ethanol reduced mean latency on the MSLT. The lowest caffeine dose reversed this effect and the highest dose increased mean latency (greater alertness) significantly beyond placebo levels. Ethanol also impaired psychomotor performance and memory. The 300-mg caffeine dose restored performance and memory measures to placebo levels. Although visual analog ratings of dizziness were increased by ethanol, they were not diminished by either caffeine dose. In conclusion, Low-dose caffeine prevented the sleepiness and performance impairment associated with a moderate dose of ethanol. Thus, caffeine, similar to other stimulants, can reverse the physiologically sedating effects of ethanol, although other negative effects remain.