DOES THE SEDATION RESULTING FROM SLEEP-DEPRIVATION AND LORAZEPAM CAUSE SIMILAR COGNITIVE DEFICITS

It is notoriously difficult to assess the contribution of the sedative effects of benzodiazepines to the cognitive impairments that they pro duce. The purpose of the present experiment was to determine whether a similar pattern of cognitive impairment would be seen in conditions w hen subjects felt equally sleepy as the result of sleep deprivation. T he effects of a sedative dose of lorazepam (2.5 mg) in healthy volunte ers was therefore compared with the effects of acute sleep deprivation (a night on-call) in a group of junior doctors and the effects of chr onically disturbed sleep due to snoring. Lorazepam, acute sleep depriv ation, and chronic sleep disturbance all significantly increased subje ctive sedation. In addition, lorazepam significantly impaired performa nce in two tests of psychomotor speed and caused significant anterogra de amnesia. Semantic and short-term memory were not impaired by loraze pam, nor was there any impairment in executive function. The only defi cit found following acute sleep deprivation was in a test of semantic memory, generating examples from a difficult category. The only signif icant deficit in the group suffering from chronically disturbed sleep, compared with age-matched controls, was in executive function, and th ere was a nearly significant impairment in sustained attention. These results suggest that, despite the common factor of increased subjectiv e sedation, the profile of cognitive impairment in the two sleep depri vation groups are neither similar to each other nor to that seen follo wing an acute dose of lorazepam. (C) 1998 Elsevier Science Inc.