***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: 1 . The acute and subchronic effects of dothiepin 75 - 150 mg and fluoxetine 20 mg on critical fusion frequency ( CFF ) , sustained attention and actual driving performance were compared with those of placebo in a double-blind , cross-over study involving 18 healthy volunteers .  Drugs and placebo were administered for 22 days in evening doses . Fluoxetine doses were constant but dothiepin doses increased on the evening of day 8 . Performance was assessed on days 1 , 8 and 22 of each treatment series . Subjective sleep parameters and possible side effects were recorded on visual analogue scales on alternate treatment days . 2 . Dothiepin  reduced sustained attention on day 1 by 6.7 % ( 95 % confidence interval ( C1 ) : -12.0 to -1.3 % ) and CFF on day 22 by 1.1 ( CI : -2.2 to -0.1 ) Hz . Fluoxetine reduced sustained attention days 1 , 8 and 22 of treatment by 7.4 , 6.7 and 6.5 % respectively ( CI : -11.3 to -3.6 ; -14.3 to -1.5 and -9.5 to -3.4 ) . CFF decreased linearly over days during fluoxetine treatment and significantly differed from placebo on day 22 with 1.2 Hz ( CI : -2.3 to -0.2 ) . Neither drug significantly affected driving performance . Whilst receiving dothiepin , subjects complained of drowsiness on days 1 - 3 of treatment ( mean rank 5.6 ; CI : 2.0 to 9.2 ) and slept 43 min longer ( CI : 8.2 to 76.2 ) . ( ABSTRACT TRUNCATED AT 250 WORDS Parallel groups of depressed ( DSM III-R ) out patients received moclobemide ( n = 22 ) and fluoxetine ( n = 19 ) , double blind , for 6 weeks . Respective starting doses were 150 mg twice a day and 20 mg q.a.m . These could be doubled after 3 weeks for greater efficacy . Chronic users of benzodiazepine anxiolytics continued taking them as comedication . Therapeutic and side effects were assessed using conventional rating scales . Actual driving performance was assessed during the week before therapy and at 1 , 3 and 6 weeks thereafter using a st and ardized test that measures st and ard deviation of lateral position ( SDLP ) . Similar remissions in depressive symptoms and side effects occurred in both groups . Patients drove with normal and reliable ( r = 0.87 ) SDLPs before treatments . Most continued to do so but a few drove with progressively rising SDLPs and the overall trends were significant in both groups ( p < 0.03 ) . A post-hoc multiple regression analysis was applied for identifying factors that correlated with SDLP in separate tests after the beginning of therapy . At 3 and 6 weeks there were significant ( p < 0.03 ) relationships involving the same factor ; patients who drove with progressively higher SDLPs appeared to be those using benzodiazepines that are metabolized by a P450 isozyme subject to inhibition by their particular antidepressant OBJECTIVE To assess the effects of paroxetine and mirtazapine on psychometric performance related to car driving , including an on-the-road test of BRT . METHOD In a 4-way , double blind r and omised crossover study , 12 healthy volunteers received paroxetine 20 mg mane , mirtazapine 15mg/30 mg nocte ( comparator ) , mirtazapine 15 mg mane/15 mg b.i.d.(verum ) and placebo over a 5 day period with a washout period of 7 days between treatments . Psychometric assessment s included ' on-the-road ' BRT ( BRT ) , CFF ( CFF ) , CRT ( CRT ) and subjective measures of sedation and sleep parameters . RESULTS Paroxetine had no significant effect on BRT compared with placebo . Although subjective ratings of sleep quality and sedation were impaired , there were significant improvements in both CFF and the recognition reaction component of CRT with paroxetine . Mirtazapine 15mg/30 mg nocte impaired laboratory performance and some subjective tests .  Mirtazapine 15 mg mane/15 mg b.i.d . improved sleep , but significantly impaired all other measures . CONCLUSION Paroxetine 20 mg/day has no psychomotor or behavioural toxicity and has no negative impact on BRT . Further research into the chronic and sub-chronic effects of mirtazapine is needed to establish the clinical significance of these results OBJECTIVE The aim of the present study was to examine the influence of reboxetine and mirtazapine on psychomotor functions related to driving skills and on driving simulator performance in depressed in patients . METHOD Forty depressed in patients diagnosed according to DSM-IV-TR criteria were r and omly assigned to treatment with either reboxetine ( N = 20 ) or mirtazapine ( N = 20 ) . To control for retest effects in psychomotor measures , a group of 10 healthy controls was examined on the same time schedule . Participants were tested once before pharmacologic treatment and twice after initiation of treatment ( days 7 and 14 ) with computerized tests related to car-driving skills .  Data were collected with the Act and React Testsystem ART-90 and the Wiener Testsystem , measuring visual perception , reactivity , stress tolerance , concentration , and vigilance . In addition , patients went through various risk simulations on a static driving simulator . Data were analyzed with nonparametric statistics and repeated- measures analysis of variance . The study was conducted from June 2004 through June 2006 . RESULTS Before onset of treatment with antidepressants , about 65 % of patients did not reach the threshold criterion according to the German guidelines for road and traffic safety . After 14 days of treatment with reboxetine or mirtazapine , patients improved in driving ability skills . Controlling for retest effects in psychomotor measures , data indicate that both patient groups significantly improved in tests measuring selective attention and reactivity ( all p < .01 ) . Furthermore , the frequency of accidents in the risk simulations markedly decreased in patients receiving mirtazapine and reboxetine ( all p < .05 ) . Statistically significant differences between treatment groups could not be shown . CONCLUSION Our results indicate that partially remitted depressed in patients treated with reboxetine or mirtazapine show a better performance on tasks related to driving skills than do untreated depressives The effects of paroxetine ( 20 and 40 mg/day ) and amitriptyline ( 75 mg/day , used as an active control ) on car driving and psychomotor function were compared with those of placebo in a double-blind , crossover study employing 16 healthy subjects . Performance testing occurred on the first and last day of each 8-day treatment series . Side-effects , sleep duration and sleep quality were rated daily . Amitriptyline produced severe drowsiness and strikingly impaired performance on nearly every test on the first day but its effects were practically gone after 1 week of treatment . Paroxetine 20 mg , the usual antidepressant dose , had no effect on performance .  Paroxetine 40 mg did not affect road tracking but slightly impaired performance in some psychomotor tests in a persistent manner . Paroxetine had no effect on sleep following the 20 mg dose but reduced quality following the 40 mg dose . Side-effects that the administered drugs have in common were milder during paroxetine than amitriptyline treatment . However , some dose-related side-effects ( e.g. nausea and delayed ejaculation ) were only reported during paroxetine treatment This was a placebo-controlled , double-blind r and omized crossover study of long-term ( 5 weeks ) administration of fluoxetine ( 20 mg/day ) and dothiepin ( 75 mg/day for 1 week followed by 150 mg/day for 4 weeks ) in 12 healthy male volunteers . Subjects were studied on day 10 and day 36 of treatment , with tests of nocturnal sleep , driving performance , continuous electroencephalogram ( EEG ) , sleep during scheduled naps , computerized visual attention tasks , saccadic eye movement measurement and visual analogue ratings of mood . Both drugs had a marked suppressive effect on nocturnal rapid eye movement ( REM ) sleep ; these effects were less at 36 days than at 10 days , and fluoxetine decreased and dothiepin increased REM in daytime naps . Sleep fragmentation after fluoxetine is similar to that reported in the literature . We found no sleep-promoting effects of dothiepin , in contrast to our previous single-dose study , and no subjective sleep effects of either drug . Subjects were less sleepy after both antidepressants than placebo at 5 weeks measured by sleep latencies and EEG . Saccadic eye movement measures were significantly faster after 5 weeks of fluoxetine than after 5 weeks of placebo .  Reaction times to a peripheral stimulus during computerized tracking task were shorter after 10 days of dothiepin compared with placebo .  Driving performance , visual attention and mood ratings showed no treatment effects . Subjective health reports during each 5 weeks of treatment were similar in number for the two drugs but showed a different profile of side-effects The effects of fluvoxamine ( 50 or 100 mg ) , alone and in combination with ethanol ( 0.8 g/kg ) , on psychomotor and cognitive performance and on autonomic nervous system reactivity were studied in healthy male volunteers .  Fluvoxamine produced neither serious psychomotor or cognitive impairment nor alterations in autonomic nervous system functioning at these doses . There was no evidence that fluvoxamine exacerbated , or improved , ethanol-induced impairments of memory or any other measures evaluated . Fluvoxamine tended to improve recognition , but not free recall , of words A double-blind , placebo-controlled , crossover study in 12 subjects ( greater than or equal to 50 years ) compared the effects of single oral doses of sertraline ( 100 mg ) and amitriptyline ( 50 mg ) with placebo as assessed by psychomotor function testing . Unlike sertraline and placebo , amitriptyline increased tracking error severity and impaired digit/symbol substitution .  Sertraline slightly improved flicker frequency recognition . Both active drugs caused subjective drowsiness , although amitriptyline 's effect was greater and of longer duration . Both drugs impaired subjectively assessed performance .  Sertraline caused nausea , and  amitriptyline  , dry mouth ;  sertraline tended to increase supine systolic blood pressure . The authors conclude that sertraline has a considerably less detrimental effect on psychomotor performance and may have a slight activating effect not found with amitriptyline OBJECTIVE Psychomotor disturbances can frequently be found in depressed patients and may have an important influence on the ability to drive . Additionally , effects of sedation , as seen with some antidepressants , probably impair driving performance . The present study was design ed to evaluate the effects of antidepressant monotherapy on psychomotor functions related to car-driving skills in depressive patients in a routine clinical setting . METHOD In patients ( N = 100 ) who met the ICD-10 and DSM-IV criteria for major depressive disorder were tested under steady-state plasma level conditions prior to being discharged to out-patient treatment . The study ran from January 2004 through March 2005 . All patients participated voluntarily and gave informed consent . According to the German guidelines for road and traffic safety , data were collected with the computerized Act & React Testsystem ART-90 and the Wiener Testsystem , measuring visual perception , reaction time , selective attention , vigilance , and stress tolerance . Psychopathologic symptoms were rated with the Hamilton Rating Scale for Depression . RESULTS Before discharge to outpatient treatment , 24 % of the patients tested were without clinical ly relevant psychomotor disturbances . In 60 % of the cases , mild to moderate impairments could be seen , and about 16 % of the patients were considered as severely impaired in psychomotor functions related to car-driving abilities . Data show that patients treated with selective serotonin reuptake inhibitors ( SSRIs ) or the noradrenergic and specific serotonergic antidepressant ( NaSSA ) mirtazapine had an altogether better test performance in comparison with patients receiving tricyclic antidepressants ( TCAs ) . Differences were most pronounced in measures of reactivity , stress tolerance , and selective attention . Statistically significant differences between patients treated with TCAs or the serotonin-norepinephrine reuptake inhibitor ( SNRI ) venlafaxine could not be found . Among the newer antidepressants there is an advantage for patients treated with mirtazapine , especially in tasks with high multi-channel perception and output dem and s. CONCLUSION About 16 % of depressive patients discharged from hospital to outpatient treatment must be considered unfit to drive . In 60 % of the cases , patients performed at a question able level of fitness for driving , and it seems justified to counsel patients individually , taking into account compensational factors . Data point to an advantage for patients treated with SSRIs or mirtazapine when compared with TCAs or venlafaxine . However , causal relationships can not be drawn from our data OBJECTIVE The effects of escitalopram 10 to 20 mg/day and mirtazapine 30 to 45 mg/day on actual driving and psychomotor performance of 18 healthy subjects were determined in a r and omized , double-blind , placebo-controlled , multiple-dose , 3-way 
    Output:
    
There is evidence that the SSRIs ( citalopram , escitalopram , fluoxetine , fluvoxamine , sertraline , paroxetine ) and the SNRI venlafaxine have no deleterious effects on driving ability .
Acute use of mirtazapine does produce impairments that diminish to some degree when given as a nocturnal dose and can not be seen after repeated dosing in healthy controls .
Patients obviously benefit from treatment with newer antidepressants ; however , at least a subgroup does not reach performance level of healthy subjects .