This study evaluated the effects of flurazepam 30 mg, lorazepam 4 mg, triazolam 0.5 mg, and placebo upon sleep and memory in eleven normal male subjects continuously monitored for nighttime EEG, EOG, and EMG recording. Subjects received each drug or placebo for two consecutive nights per week for 4 weeks in a repeated measures, double-blind, Latin Square design. Three hours post-administration, subjects were awakened and presented with a series of tasks. Recall was assessed immediately following task presentation and after the final morning awakening. The results showed that every drug significantly decreased stage 1, increased stage 2, and produced no change in stage 3--4 sleep in comparison to placebo. Only lorazepam significantly decreased REM percent. Post-drug recall was significantly decreased in comparison to placebo at night and was further decreased in the morning. Morning recall was significantly poorer when the return to sleep was 2.5 min or less than when the return to sleep was greater than 5 min following the nighttime awakening in all drug conditions. These results indicate that 1. failure of memory consolidation rather than failure of retrieval is the most likely explanation for the morning memory loss and 2. hypnotic drug properties, measured by latency to fall back asleep, affect memory consolidation.
"Long-term memory deficits (morning recall in our methodology) could be the result of failure of memory consolidation at night or failure of memory retrieval in the morning. In the first study we found that morning recall was correlated (r = 0.74) with the latency to fall back asleep after the night-time awakening (Roth et al., 1980). Figure 1 illustrates the correlation. "
[Show abstract][Hide abstract] ABSTRACT: Benzodiazepines possess anterograde amnesic properties, disrupting both short-term and long-term memory function. The amount of amnesia is systematically related to dose effects and half-life differences among the benzodiazepines. Memory deficits are found for episodic, semantic, and iconic memory function. The deficits in long-term memory are probably the result of a disruption of consolidation of information in memory and not retrieval from memory. The disruption is produced by rapid sleep onset. Thus the long-term amnesia is really a retrograde effect of sleep and not the anterograde effect of the drug.
British Journal of Clinical Pharmacology 02/1984; 18 Suppl 1(S1):45S-49S. DOI:10.1111/j.1365-2125.1984.tb02581.x · 3.88 Impact Factor
"No significant changes in EEG parameters related to sleep efficiency index, total sleep time, sleep onset latency, and number of awakenings could be detected . These results are consistent with earlier studies (Roth et al., 1980; Kales et al., 1986; Röschke et al., 1993), where it has been shown that under the influence of lorazepam the percentage of stage II increased, whereas the percentage of REM sleep was reduced to nearly half of its baseline values under drug free conditions. However, the aim of the present paper was to investigate the sleep EEG's microstructure under the influence of the benzodiazepine lorazepam. "
[Show abstract][Hide abstract] ABSTRACT: Background: When searching for reliable and specific markers for certain psychiatric diseases, prelimi- nary investigations of the sleep EEG's microstructure point to the view that the delta/beta correlation coefficients during NREM sleep appear increased in depressives, but not in schizophrenics. Therefore, this parameter could be hypothesized to be a marker of depression. On the other hand, subchronically, paroxetine medication in healthy subjects produces the opposite finding: a decrease in the delta/beta correlation coefficients during NREM sleep, which might be interpreted as evidence of the antidepres- sant action of the drug. Of course, a close connection between this effect and the antidepressant effi- cacy of this drug has not been demonstrated to date. Objective: The aim of the present paper was to il- luminate the sleep EEG's microstructure under the influence of the benzodiazepine lorazepam. This drug influences the conventional sleep EEG parameters very similarly to most of the antidepressants. However, it should be assumed that benzodiazepines do not act as antidepressants. Therefore, the question arises as to whether lorazepam alters the delta/beta correlation of the sleep EEG in the same way as paroxetine. Method: Separately for REM and NREM sleep we calculated the correlation coef- ficients between different frequency bands (delta, theta, alpha, beta) from sleep EEG data of healthy subjects (n=8) from Pz-Cz through the night in a double-blind placebo-controlled cross-over design (single dose of 2.5 mg lorazepam). Results: Despite the alterations of the conventional sleep EEG parameters, no influence of lorazepam on the sleep EEG's microstructure could be observed. Conclusions: Assum- ing the findings of the present paper can be replicated in a larger sample size, NREM alterations of the sleep EEG's delta/beta oscillations may be characteristic for depression and antidepressants (German J Psychiatry 2000;3:13-18)
[Show abstract][Hide abstract] ABSTRACT: Midazolam, an investigational hypnotic, was evaluated for effectiveness, side effects, and withdrawal phenomena in doses of 10, 20, and 30 mg in three separate sleep laboratory studies, each including 4 placebo-baseline nights, 7 drug nights, and 3 placebo-withdrawal nights. Only a slight to moderate degree of effectiveness was shown across the three doses; this effectiveness was much more pronounced during the first third of the night. There was no dose-response effect for effectiveness with either initial or continued drug administration. In general, there was less effectiveness on the last 3 drug nights, indicating a potential for the development of tolerance over a relatively short period of time. Following withdrawal there was a marked dose-related worsening of sleep above baseline levels (rebound insomnia).
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