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.

The validity of actigraphy to make this distinction relative to polysomnography depends on several factors, including the population being studied and the time-of-day. In healthy, normal young, and middle-age adults sleeping at night, the agreement between actigrahpic and polysomnographic assessment of sleep time is generally 90% and better. 1 In contrast, in the elderly and patients with sleep disorders, the percent agreement generally is less, sometimes 80% or lower. 1 The discrepancy is in both directions with over-and under-estimations of sleep time. Some elderly and patients often lie motionless while awake producing over-estimation of sleep time, while other patients may have many body movements or leg movements during sleep producing under-estimations of sleep time.As to time-of-day, detecting sleep episodes with actigraphy in the context of normal waking activity has not been successful. In healthy young adults actigraphy differentiated sleep and wake at night, but it did not do so during daytime napping. 2 The agreement between actigraphic and polysomnographic identification of sleep was 40%. Periods of inactivity while reading or watching TV could not be differentiated from daytime nap episodes.While actigraphy may not detect daytime sleep episodes, it may differentiate increasing levels of daytime sleepiness as reflected in reduced overall activity or increased brief periods of inactivity. Reducing sleep time in healthy normals increases the level of daytime sleepiness in a linear manner as measured by the Multiple Sleep Latency Test (MSLT). 3,4 Increased daytime sleepiness then may be associated with reduced activity. We know of no previous attempts to document with actigraphy differing levels of daytime sleepiness due to reduced bedtime the previous night. Since previous studies have shown increased sleepiness and reduced performance following sedating drugs, the antihistamine diphenhydramine was used as a positive control in this study. 5,6 Thus, this study compared the effect of sleep loss, due to reduced sleep times, with the effect of diphenhydramine 50 mg on the MSLT and waking actigraphy. It was hypothesized that sleep loss the previous night would reduce activity levels during the following day. Each day the volunteers wore actigraphs from 0700-1800 hrs. Decreasing TIB was associated with decreased daily mean sleep latency on the MSLT with 4 and 0 hrs differing from 8 hrs and each other. Daytime activity also was reduced by the reduced prior TIB. Increased inactivity relative to the 8 hr TIB developed between the 4 hr and 0 hr TIBs, with 4 hrs differing from 0 hrs, but not 8 hrs. Accepted for publication June 2000Diphenhydramine 50 mg reduced mean daily sleep latency and increased percent inactive time relative to placebo. On the MSLT diphenhydramine was intermediate to 4 hr and 0 hr TIB and on actigraphy it was similar to 0 hr TIB. Conclusions:The difference in the effect of diphenhydramine on these actigraphy and MSLT may reflect the different sensitivities of the measures.

So that reinforcing and subjective effects of methylphenidate as a function of dose and level of sleepiness could be evaluated, 21 volunteers received methylphenidate (5, 10, or 20 mg) or placebo on 2 sampling days. After 4 and 8 hr time in bed (TIB), they chose their preferred capsule on 5 days. Methylphenidate was chosen more frequently after 4 hr TIB (60%) than it was after 8 hr TIB (33%). The strongest preference (68%) was seen in the 10-mg group. At 10 and 20 mg, stimulant-like subjective effects were reported. The 10-mg group was more adversely affected by the restricted bedtime and showed more pronounced drug effects with methylphenidate. These results indicate that sleepiness modulates the reinforcing and subjective effects of methylphenidate.

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