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An investigation of the range of cognitive impairments induced by scopolamine 0·6 mg s.c
Author(s) -
Wesnes K.,
Simpson P.,
Kidd A.
Publication year - 1988
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.470030106
Subject(s) - alertness , vigilance (psychology) , recall , cognition , psychology , placebo , working memory , audiology , scopolamine , cholinergic , scopolamine hydrobromide , effects of sleep deprivation on cognitive performance , memoria , flicker fusion threshold , cognitive psychology , developmental psychology , neuroscience , medicine , anesthesia , muscarinic acetylcholine receptor , computer science , psychiatry , alternative medicine , receptor , pathology , flicker , operating system
The present study was conducted to determine the degree to which impairments in attention accompany the memory deficits produced by scopolamine. Eighteen healthy young volunteers received scopolamine 0·6 mg subcutaneously on three experimental sessions and placebo on three others. On each session, prior to, and 60 min after injection, the subjects underwent an automated computerized battery of 11 cognitive tasks. The study was run double‐blind and the order of treatment conditions over successive visits was counterbalanced between subjects. Scopolamine produced marked and significant decrements on all major aspects of performance from the battery. The drug lowered the efficiency of the detection and processing of information in tests of visual vigilance, rapid information processing, choice reaction, letter cancellation and logical reasoning. These effects were accompanied by a lowering of critical flicker‐fusion frequency and subjective alertness. Memory was also impaired on tests of immediate recall, delayed recall, recognition and memory scanning. These findings confirm and extend previous work, demonstrating that scopolamine impairs the selection and evaluation of environmental information, as well as reducing the likelihood of information being subsequently recalled or recognized. Whether the former effects contribute to the latter is not known, but this must be considered a possibility. This potential role of processing deficits in memory loss associated with cholinergic blockade is briefly considered in relation to the cholinergic hypothesis of geriatric memory loss.