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There is little empirical research on the familial and parental correlates of alexithymia. A two-part study explored how the affective and cognitive characteristics of alexithymia are related to family dysfunction and maternal alexithymia. In Part I, 127 young adults were evaluated for alexithymia with the Toronto Alexithymia Scale-20 (TAS-20), for impaired imagination with the Scored Archetypal Test with Nine Elements, and for family dysfunction with the McMaster Family Assessment Device. In Part II, 80 of their mothers completed the TAS-20 about themselves, and maternal alexithymia characteristics were correlated with those of their offspring. In Part I, general family pathology was associated with alexithymia. In particular, difficulty identifying feelings was related to dysfunctional family affective involvement, externally oriented thinking was related to deficient family behavior control, and impaired imagination was related to inadequate family problem solving; these relationships were independent of general family pathology and subjects' positive and negative affect. In Part II, maternal alexithymia characteristics were correlated significantly with the offsprings', controlling for both respondents' positive and negative affect. These findings implicate disturbed family functioning and maternal alexithymia in the development of alexithymia characteristics in children.

On 4 days, 6 volunteers received 10 mg methylphenidate or placebo at 0900 after 4 or 8 hr time in bed (TIB) and then on 4 days after 4 or 8 hr TIB chose their preferred capsule. On sampling days, 4 hr TIB increased multiple sleep latency test (MSLT) scores and Fatigue scale scores on the Profile of Mood States (POMS). In both TIBs, the drug increased the MSLT and POMS Vigor and Tension scale scores. It reduced POMS Fatigue scores and improved divided attention performance to a greater extent after 4 versus 8 hr. Drug was chosen on 88% of days after 4 hr, but only 29% of days after 8 hr. Preference for the drug depends on sleepiness and is mediated by performance-enhancing and fatigue-altering effects.

The Multiple Sleep Latency Test (MSLT) was used to assess the effects of ethanol at the peak and descending phases of the breath ethanol curve. Ethanol (0.75 g/kg) was administered (at 0900 hr) to 8 healthy, normal-sleeping men, aged 21 to 45 years old after 8 hr of sleep the previous night. MSLTs were conducted and breath ethanol concentrations (BrECs) were measured at 15, 45, 75, 105, 225, and 345 min after drinking was completed. Subjective measures were administered immediately before each sleep latency test. BrECs over the first 75 min (tests 1 to 3) peaked and differed from all subsequent tests (tests 4 to 6) over which BrECs declined. Sleep latency and subjective measures were averaged over tests 1 to 3 and 4 to 6. There was a significant increase in mean sleep latency relative to placebo for tests 1 to 3 and a significant reduction for tests 4 to 6. The subjective measure of stimulation sedation, the Biphasic Alcohol Effects Scale, showed lessened sedation after ethanol versus placebo on tests 1 to 3, compared with tests 4 to 6. This study confirmed the presence of a biphasic ethanol effect using an electrophysiological method (MSLT), showing increased physiological alertness on the peak phase of the BrEC curve and increased sedation on the descending phase. Relative to the effects observed on the MSLT with other low-dose stimulant drugs, the stimulatory effect of ethanol was mild.