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The depressed patients were classified according to the DSM‐III into minor, simple major and major depression with melancholia. We found a significant, enhacing effect for L‐TRP on urinary free cortisol (UFC) excretion. The absolute increments in UFC induced by L‐TRP were significantly higher in melancholic females as compared to minor and simple major depressives. 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Study 1 (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 47) compared zaleplon (10 and 40 mg) to triazolam (0·25 mg) and placebo. Study 2 (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 36) compared zaleplon (20 and 60 mg) to triazolam (0·25 mg) and placebo. For each study, polysomnographically recorded sleep parameters and patient reports of sleep quality were collected during baseline and two consecutive nights during the four treatment phases in each study. All doses of zaleplon produced significant decreases in latency to persistent sleep. Although no minimally effective dose could be determined, dose‐response effects were apparent. Triazolam 0·25 mg produced a decrease in latency to persistent sleep that was comparable to that of zaleplon 10 mg. Only the triazolam dose and the 60 mg dose of zaleplon produced significant increases in total sleep time over placebo. Zaleplon 40 and 60 mg and triazolam produced decreases in the percentage of REM sleep compared to placebo. Patient reports of efficacy were consistent with objective findings. In addition, all doses of zaleplon tended to increase while triazolam decreased the percentage of stage 3\u002F4 sleep. There was no evidence of residual daytime impairment for any of the zaleplon doses, however, triazolam administration produced significant impairment in performance on a digit copying test. A higher number of adverse events were seen with the 40 and 60 mg doses of zaleplon compared to triazolam (0·25) and placebo. At higher doses, zaleplon is more effective than triazolam at reducing latency to persistent sleep in chronic insomnia and is not associated with the decrease in slow‐wave sleep or residual impairment observed with triazolam. However, increases in total sleep time were apparent only at doses which produced concomitant increases in the number of adverse events. In contrast, triazolam (0·25 mg) produced increases in total sleep time (˜25 min) and decreases in latency to persistent sleep at a dose of 0·25 mg. 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II [In Process Citation], Sleep, 22, S354",{},{"id":24,"text":954,"url":24,"identifiers":955},"Roth T, 1980, The differential effects of short‐ and long‐acting benzodiazepines upon nocturnal sleep and daytime performance, Arzneimittelforschung, 30, 891",{},{"id":24,"text":957,"url":24,"identifiers":958},"10.1111\u002Fj.1365-2125.1979.tb00456.x",{"doi":957},{"id":24,"text":960,"url":24,"identifiers":961},"10.1016\u002FS0091-6749(87)80197-5",{"doi":960},{"id":24,"text":963,"url":24,"identifiers":964},"10.1093\u002Fsleep\u002F18.4.246",{"doi":963},{"id":24,"text":966,"url":24,"identifiers":967},"Roth T, 1991, A review of the safety profiles of benzodiazepine hypnotics, J Clin Psychiatry, 52, 38",{},{"id":24,"text":969,"url":24,"identifiers":970},"10.1002\u002Fj.1875-9114.1983.tb03237.x",{"doi":969},{"id":24,"text":972,"url":24,"identifiers":973},"Scharf MB, 1994, A multicenter, placebo‐controlled study evaluating zolpidem in the treatment of chronic insomnia, J Clin Psychiatry, 55, 192",{},{"id":24,"text":975,"url":24,"identifiers":976},"10.1176\u002Fajp.154.10.1417",{"doi":975},{"id":24,"text":978,"url":24,"identifiers":979},"Spitzer RL, 1987, Diagnostic and Statistical Manual of Mental Disorders",{},{"id":24,"text":981,"url":24,"identifiers":982},"10.2165\u002F00044011-199816050-00001",{"doi":981},{"id":24,"text":984,"url":24,"identifiers":985},"10.1016\u002FS0163-8343(97)00056-X",{"doi":984},{"id":987,"createTime":988,"updateTime":988,"relativeEntities":989,"slug":990,"properties":991,"entityType":128,"verifyStatus":129,"verifyTime":1004,"verifyNote":130,"languages":1005,"translateLanguages":24,"viewCount":25,"primaryUrl":1006,"fullTextUrl":24,"authors":1007,"publicationType":202,"publisherRelationship":1061,"citationCount":1119,"citationInfo":1120,"publishDate":1123,"publishYear":1121,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1124,"openAccess":24,"references":1125,"isForceReanalyzing":360},"5e3693da-3574-47c2-9a8e-86e076095a3f","2024-11-26T20:05:35.890+00:00",[],"Nicotine-improves-antisaccade-task-performance-without-affecting-prosaccades",{"openalex":992,"mag":994,"abstract":996,"title":998,"pm":1000,"doi":1002},{"VOID":993},"W2014882990",{"VOID":995},"2014882990",{"EN":997},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Although there is ample evidence for a cognitive‐attentional benefit of the stimulant nicotine, the source of this benefit is not as well understood. One approach is to address what aspects of performance nicotine affects at a functional systems level. It is currently debated whether the benefits produced by nicotine are the effect of enhanced higher cognitive function or reflect an overall increase in general arousal. In order to address this question, the effects of nicotine on two simple eye movement tasks were studied: the saccade (S) and antisaccade (AS) tasks. Because the S and AS tasks utilize identical sensory stimuli (peripheral targets) and require identical motor responses (eye movements) but differ significantly in their cognitive demands, the use of these two tasks should enable a parsing of nicotine effects on cognitive versus sensory‐motor processes. In this study, the S and AS tasks were performed by two experimental groups, task naïve subjects and highly practised subjects. For the first group, that of the task naïve subjects, nicotine gum administration resulted in a decrease in AS errors. For the second group, that of two experienced subjects tested repeatedly over a 3 week period, nicotine also produced a significant decrease in AS task errors, as well as resulting in a significant decrease in AS response times. Neither task naïve nor experienced subjects showed any effects of nicotine on the S task. Examining the effects of nicotine on highly controlled and constrained tasks such as the S and AS task may provide another level of insight into the mechanisms underlying the beneficial cognitive effects of nicotine. Copyright © 2004 John Wiley & Sons, Ltd.\u003C\u002Fjats:p>",{"EN":999},"Nicotine improves antisaccade task performance without affecting prosaccades",{"VOID":1001},"15303245",{"VOID":1003},"10.1002\u002Fhup.604","2024-11-26T20:05:35.889+00:00",[132],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fhup.604",[1008,1025,1042],{"id":1009,"sortIndex":25,"researcher":24,"roles":1010,"affiliations":1011,"properties":1020,"displayName":1022,"givenName":24,"familyName":24},"672ccd00-9ce0-4710-a029-07a8773abca6",[],[1012],{"id":1013,"sortIndex":25,"affiliation":1014,"properties":24},"cc5443c3-deba-4409-9b7e-ac7810f8b787",{"id":1013,"createTime":24,"updateTime":24,"relativeEntities":1015,"slug":24,"properties":1016,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1019,"statistic":24},[],{"title":1017},{"EN":1018},"Department of Neurobiology and Anatomy, University of Texas-Houston Medical School, 6431 Fannin, Houston, TX 77030, USA.",[],{"title":1021,"openalex":1023},{"EN":1022},"Abigail L. 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Psychiatry, 45, 204",{},{"id":1297,"createTime":1298,"updateTime":1298,"relativeEntities":1299,"slug":1300,"properties":1301,"entityType":128,"verifyStatus":129,"verifyTime":1298,"verifyNote":130,"languages":1316,"translateLanguages":24,"viewCount":25,"primaryUrl":1317,"fullTextUrl":24,"authors":1318,"publicationType":202,"publisherRelationship":1357,"citationCount":1415,"citationInfo":1416,"publishDate":1428,"publishYear":1417,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1429,"openAccess":24,"references":1430,"isForceReanalyzing":360},"e19b357e-3276-4317-af30-7571828abab3","2024-11-26T00:05:26.594+00:00",[],"Circadian-rhythm-disturbances-in-depression",{"mag":1302,"pmc":1304,"openalex":1306,"abstract":1308,"title":1310,"pm":1312,"doi":1314},{"VOID":1303},"2104247936",{"VOID":1305},"2612129",{"VOID":1307},"W2104247936",{"EN":1309},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Objective\u003C\u002Fjats:title>\u003Cjats:p>The aim of this article is to review progress in understanding the mechanisms that underlie circadian and sleep rhythms, and their role in the pathogenesis and treatment of depression.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Literature was selected principally by Medline searches, and additional reports were identified based on ongoing research activities in the authors' laboratory.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Many physiological processes show circadian rhythms of activity. Sleep and waking are the most obvious circadian rhythms in mammals. There is considerable evidence that circadian and sleep disturbances are important in the pathophysiology of mood disorders. Depressed patients often show altered circadian rhythms, sleep disturbances, and diurnal mood variation. Chronotherapies, including bright light exposure, sleep deprivation, and social rhythm therapies, may be useful adjuncts in non‐seasonal and seasonal depression. Antidepressant drugs have marked effects on circadian processes and sleep.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>Recent progress in understanding chronobiological and sleep regulation mechanisms may provide novel insights and avenues into the development of new pharmacological and behavioral treatment strategies for mood disorders. Copyright © 2008 John Wiley & Sons, Ltd.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":1311},"Circadian rhythm disturbances in depression",{"VOID":1313},"18680211",{"VOID":1315},"10.1002\u002Fhup.964",[132],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fhup.964",[1319,1338],{"id":1320,"sortIndex":25,"researcher":24,"roles":1321,"affiliations":1322,"properties":1331,"displayName":1335,"givenName":24,"familyName":24},"7cb861a7-e9ac-4622-9343-e5de5e14dbc9",[],[1323],{"id":1324,"sortIndex":25,"affiliation":1325,"properties":24},"82549cd2-7bbc-4fcd-9808-769adde7d142",{"id":1324,"createTime":24,"updateTime":24,"relativeEntities":1326,"slug":24,"properties":1327,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1330,"statistic":24},[],{"title":1328},{"EN":1329},"Department of Psychiatry, University of Pittsburgh School of Medicine,Pennsylvania 15213, USA.",[],{"orcid":1332,"title":1334,"openalex":1336},{"VOID":1333},"https:\u002F\u002Forcid.org\u002F0000-0001-6672-4800",{"EN":1335},"Anne Germain",{"VOID":1337},"A5044453237",{"id":1339,"sortIndex":156,"researcher":24,"roles":1340,"affiliations":1341,"properties":1350,"displayName":1354,"givenName":24,"familyName":24},"09107118-1493-4822-bf5a-8f02ea7b25dd",[],[1342],{"id":1343,"sortIndex":25,"affiliation":1344,"properties":24},"718ce856-cbbf-49fc-a024-b5a2d6ca5082",{"id":1343,"createTime":24,"updateTime":24,"relativeEntities":1345,"slug":24,"properties":1346,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1349,"statistic":24},[],{"title":1347},{"EN":1348},"Department of Psychiatry, University of Pittsburgh, School of Medicine, Pennsylvania, USA.",[],{"orcid":1351,"title":1353,"openalex":1355},{"VOID":1352},"https:\u002F\u002Forcid.org\u002F0000-0002-4217-8304",{"EN":1354},"David J. 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medication may impair psychomotor and cognitive function, and so increase accident susceptibility. However, few studies examine any association in the framework of other demographic, health and occupational factors.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Objectives\u003C\u002Fjats:title>\u003Cjats:p>To examine the relationship between sleeping tablets and antidepressants, and accidents, minor injuries and cognitive failures.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Postal questionnaire study of 3111 individuals who participated in an earlier phase of the Bristol Stress and Health Study.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Sleeping tablet use was associated with accidents, minor injuries and cognitive failures both at work and outside work. Antidepressant use was associated with accidents and cognitive failures both at work and outside work. Adjusting for health, demographic and occupational factors explained many of these associations, but sleeping tablet use was independently associated with accidents (both at work and outside work), and antidepressant use with cognitive failures (outside work).\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>Antidepressant and sleeping tablet use were apparently associated with accidents, minor injuries and cognitive failures. Although most of the associations could be accounted for by other factors the results suggested links between sleeping tablet use and accidents, and between antidepressant use and cognitive failures. Copyright © 2003 John Wiley & Sons, Ltd.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>",{"EN":2104},"Preliminary investigation of the association between psychotropic medication use and accidents, minor injuries and cognitive failures",{"VOID":2106},"14533135",{"VOID":2108},"10.1002\u002Fhup.516",[132],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fhup.516",[2112,2131,2146,2163],{"id":2113,"sortIndex":25,"researcher":24,"roles":2114,"affiliations":2115,"properties":2124,"displayName":2128,"givenName":24,"familyName":24},"377b528d-b73d-4129-807e-d5b6891f046c",[],[2116],{"id":2117,"sortIndex":25,"affiliation":2118,"properties":24},"9b54e048-565c-4b86-ac8c-294d5352f338",{"id":2117,"createTime":24,"updateTime":24,"relativeEntities":2119,"slug":24,"properties":2120,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2123,"statistic":24},[],{"title":2121},{"EN":2122},"Centre for Occupational and Health Psychology, Cardiff University, 63                         Park Place, Cardiff, CF10 3AS, UK,",[],{"orcid":2125,"title":2127,"openalex":2129},{"VOID":2126},"https:\u002F\u002Forcid.org\u002F0000-0001-8656-5907",{"EN":2128},"Emma Wadsworth",{"VOID":2130},"A5012181059",{"id":2132,"sortIndex":156,"researcher":24,"roles":2133,"affiliations":2134,"properties":2141,"displayName":2143,"givenName":24,"familyName":24},"b64c8f9e-ba58-44bf-ac1f-13381f6a035d",[],[2135],{"id":2117,"sortIndex":25,"affiliation":2136,"properties":24},{"id":2117,"createTime":24,"updateTime":24,"relativeEntities":2137,"slug":24,"properties":2138,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2140,"statistic":24},[],{"title":2139},{"EN":2122},[],{"title":2142,"openalex":2144},{"EN":2143},"Susanna C. 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Report no. DOT‐TSC‐IST‐88‐2. 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This is most likely due to a lack of suitable assessment tasks as well as clinicians' limited awareness of the appropriate statistical techniques for analysing cognitive change in individuals. This study investigated the application of statistical decision rules to the cognitive and behavioural measures of individual children with ADHD in order to classify a significant, positive response to medication. The previously reported data of 14 children with ADHD (combined type; ADHD‐CT) were re‐analysed to investigate changes in function following a low‐ and high‐dose of stimulant medication (2.5 mg and 7.5 mg dexamphetamine, respectively). The performances of 14 age‐, gender‐ and IQ‐matched controls was also analysed to provide an estimate of the false‐positive classification rate. Overall, the decision rule yielded a high sensitivity and high specificity to treatment response. In the high‐dose condition, 71% of children with ADHD demonstrated improvements in both cognitive and behavioural function. This study demonstrates an evidence‐based approach to evaluating concurrent cognitive and behavioural improvement in individual children with ADHD following treatment with stimulant medication. 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there is no doubt that benzodiazepine administration leads to transient cognitive impairment in healthy adults, the nature and magnitude of such impairment has not been well described. The cognitive effects of a single dose of alprazolam 0.5 and 1 mg were therefore assessed in 36 healthy adults on measures of psychomotor function, visual attention, working memory, planning and learning in a double‐blind parallel‐groups study. Measures of these different cognitive functions were selected on the basis of their brevity and because they yielded distributions of performance data that were without skew, floor or ceiling effects of range restriction (i.e. normal distributions). With data satisfying the assumptions for parametric analysis, measures of effect size could be computed in addition to significance testing, thus allowing for direct and meaningful comparison between the different performance measures used. Alprazolam 0.5 mg reduced only the speed of attentional performance although the magnitude of this reduction was large (\u003Cjats:italic>d\u003C\u002Fjats:italic> = 0.8). At 1.0 mg, impairments in psychomotor function, equivalent to that seen for attentional function at the lower dose, were observed. In addition, moderate (\u003Cjats:italic>d\u003C\u002Fjats:italic> approx = 0.5) impairments in working memory, and learning also became obvious. When considered together, these results suggest that low‐dose alprazolam primarily alters visual attentional function. At the higher dose psychomotor functions also become impaired, and it is likely that the combination of these led to the observed moderate impairments in higher level executive and memory processes. The current study also illustrates a method for directly comparing the magnitude of change in cognitive function between measures with different performance metrics. 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study examined between‐ and within‐subject stability of cognitive performance in individuals with chronic schizophrenia.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Thirty individuals with schizophrenia and 20 healthy controls matched by age, sex, education, and estimated IQ underwent repeated cognitive assessments at baseline and 30 days using computerized tests of psychomotor function, visual attention\u002Finformation processing, non‐verbal learning, and executive function.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>Compared to healthy controls, individuals with schizophrenia scored lower on all cognitive measures and demonstrated greater variability in cognitive performance. 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has been proposed that objective cognitive testing provides additional information to that collected via adverse event (AE) recordings. However, in clinical trials of compounds with potentially negative effects on cognition, the results of cognitive testing may overlap with AE recordings.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Aims\u003C\u002Fjats:title>\u003Cjats:p>To examine cognitive function in subjects who do and do not report sedation‐related AEs in a Phase I clinical trial.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>Five computerized cognitive tasks were administered to 28 healthy male volunteers enrolled in a simulated Phase I study using midazolam to induce sedation‐related AEs and cognitive dysfunction. For each subject, the magnitude of cognitive change between pre‐dose and 1 hr post‐dose assessments was calculated. Group and individual level cognitive outcome was compared between subjects who did and did not report sedation‐related AEs following administration of 1.75 and 5.25 mg midazolam.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>At both doses of midazolam, cognitive dysfunction was observed in both subject groups (i.e., those who did and did not report AEs). Analysis of individual outcomes identified consistent cognitive dysfunction among subjects who reported sedation‐related AEs. Further, in the 5.25 mg condition a subset of individuals (66.7%) who did not report sedation‐related AEs nevertheless displayed substantial cognitive dysfunction.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Conclusions\u003C\u002Fjats:title>\u003Cjats:p>Following administration of oral midazolam, there is a dissociation between sedation‐related AE recordings and performance on computerized cognitive tests of motor function, attention, strategy use and problem solving, learning and delayed recall. Inclusion of computerized cognitive tests in early phase trials may allow identification of subtle cognitive change, beyond that which is possible by self‐report and clinical observation. 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