Actual Driving Performance and Psychomotor Function in Healthy Subjects After Acute and Subchronic Treatment With Escitalopram, Mirtazapine, and Placebo

Wingen, Marleen; Bothmer, J.; Langer, Stefan; Ramaekers, Johannes G.

doi:10.4088/jcp.v66n0405

Cited by 88 publications

(92 citation statements)

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“…We cannot exclude the possibility that medications may have contributed to motor impairment; however, recent studies have suggested that treatment with SSRIs does not significantly impact motor performance in healthy subjects (Wingen et al, 2005) and treatment with atypical antipsychotics may in fact improve performance on tasks of motor and processing speed in schizophrenia patients (Keefe et al, 2004), making this an unlikely explanation for our results.…”

Section: Neurocognition In Ocd 643mentioning

confidence: 72%

Neurocognitive profile analysis in obsessive-compulsive disorder

Burdick

Robinson

Malhotra

et al. 2008

J Int Neuropsychol Soc

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Although neurocognitive deficits have been identified in obsessive-compulsive disorder (OCD), little research has focused on whether these deficits are generalized or specific to a given cognitive domain. We assessed the relative strengths and weaknesses of 26 adult patients with OCD compared to 38 age-and sex-matched healthy volunteers in domains of motor, verbal memory, visual memory, reasoning0problem solving, processing speed processing, and language. Profile analysis revealed an overall neurocognitive deficit of 1 2 _ standard deviation in OCD patients versus healthy volunteers, with relative weaknesses in motor and processing speed domains. In contrast, relative strengths were observed in language, verbal memory, and reasoning0problem solving. Our findings demonstrate neurocognitive impairment in OCD that may relate to functional outcome in this population. Findings of specific abnormalities on tasks of motor and processing speed are consistent with a hypothesized role of thalamocortical and basal ganglia regions in the pathogenesis of OCD. (JINS, 2008, 14, 640-645.)

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Section: Neurocognition In Ocd 643mentioning

confidence: 72%

Neurocognitive profile analysis in obsessive-compulsive disorder

Burdick

Robinson

Malhotra

et al. 2008

J Int Neuropsychol Soc

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“…In a recent review, concerning the effect of SSRIs in healthy individuals, 18 randomized trials using 39 different neuropsychological tests to investigate cognitive function were identified . Treatment with a SSRI was found to improve [Murphy et al 2008;Loubinoux et al 2005;Harmer et al 2004;Schmitt et al 2001;Knutson et al 1998Knutson et al , 1997, deteriorate [Riedel et al 2005;Schmitt et al 2002aSchmitt et al , 2001Fairweather et al 1997;Ramaekers et al 1995;Robbe and O'Hanlon, 1995] or have no effect on cognitive function [Peran et al 2008;Paul et al 2007Paul et al , 2002; Wingen et al 2006Wingen et al , 2005Loubinoux et al 2005;Riedel et al 2005;Siepmann et al 2003;Schmitt et al 2002aSchmitt et al , 2002bSchmitt et al , 2001Wilson et al 2002;Allen et al 1988;Fairweather et al 1997;Ramaekers et al 1995;Robbe and O'Hanlon, 1995]. It was concluded that the diverging findings could be a result of a number of methodological drawbacks.…”

Section: Introductionmentioning

confidence: 99%

A randomized trial of the effect of escitalopram versus placebo on cognitive function in healthy first-degree relatives of patients with depression

Knorr

Vinberg

Gade

et al. 2011

Therapeutic Advances in Psychopharmacology

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The effect of selective serotonin receptor inhibitors (SSRIs) on healthy individuals remains unclear. The aim of the trial was to evaluate the effect of the SSRI escitalopram on cognitive function in healthy first-degree relatives of patients with major depressive disorder (FDRs). A total of 80 FDRs were randomized to escitalopram (10 mg/day) (n ¼ 41) versus placebo (n ¼ 39) for 4 weeks. Neuropsychological tests and ratings of mood were applied at entry (T0) and at 4 weeks (T4). The main outcome measure was calculated as the change (T4T0) in a general cognition score, which was the standardized mean of 13 test measures. Mean change in the general cognition score was not significantly increased with escitalopram compared with placebo (p ¼ 0.37) or for any of the specific tests. In univariate analyses no statistically significant correlations were found between change in the general cognitive score and the variables age, sex, Hamilton depression score 17 items, Danish Adult Reading Test-45, and plasma escitalopram levels, respectively. These results suggest that treatment with escitalopram does not improve or impair cognitive function in FDRs. Improvement in cognitive function following treatment of depressed patients with SSRIs seems to be related to the effects on depressive symptoms rather than to a direct effect of the SSRI.

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“…Continuing treatment beyond 3-4 weeks tends to improve depression, and patients tend to become tolerant to sedative effects of sedating antidepressants. This is supported by limited experimental evidence that showed that young patient groups treated with sedative or non-sedative antidepressants improved their driving skills after a few [60][61][62] weeks while untreated patients did not .…”

Section: O G N I T I V E To X I C I T Y O F S E D a T I V E P S Y Cmentioning

confidence: 72%

Cognitive toxicity: from pesticides to pharmaceuticals

Dassanayake

2017

SL J. Med.

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Impairment of cognitive functions following neurotoxic exposure is collectively termed cognitive toxicity. This oration is based on a series of studies carried out over last 12 years on cognitive toxicity of two groups of substances, viz. organophosphate (OP) pesticides and sedative psychotropic drugs.OP pesticide poisoning is a major clinical and public health problem in South Asia. OPs act as cholinesterase inhibitors, and bring about acute neurological deficits following exposure. Using neurophysiological and neuropsychological techniques, we assess long-term neurocognitive deficits of OPs, a less known yet important adverse effect of OP exposure. The findings hitherto indicate both acute large-dose poisoning and subclinical occupational exposure are associated with long-term cognitive impairment.In the same way the pesticide use and misuse are common in agricultural communities, use and misuse of sedative psychotropic medications are common in urbanised societies. Sedative drugs, even in therapeutic doses impair driving and underlying cognitive functions, and increase the risk of traffic accidents. When taken in overdose, these drugs have cognitively impairing effects that last beyond clinical recovery from acute poisoning. These patients are more prone to traffic crashes at least up to 4 weeks following exposure, and the cognitive recovery over this period mirrors the crash risk at different post-overdose time points. The above findings raise a number of clinical and medico legal implications in post-discharge management of patients with sedative drug overdose.As the agricultural communities transform into urban industrialised societies in Sri Lanka, the pattern of poisoning changes from agrochemicals into pharmaceuticals, particularly psychotropic dugs. The two lines of research discussed above highlight how this changing social fabric poses new challenges for the neurophysiologists, neurologists and psychiatrists who study cognition and apply their findings in clinical settings. Our latest work in generating age-, sex-and education-adjusted norms for cognitive tests for Sri Lankans, would set the foundation in interpreting the cognitive test results of clinical populations.

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Actual Driving Performance and Psychomotor Function in Healthy Subjects After Acute and Subchronic Treatment With Escitalopram, Mirtazapine, and Placebo

Cited by 88 publications

References 0 publications

Neurocognitive profile analysis in obsessive-compulsive disorder

Neurocognitive profile analysis in obsessive-compulsive disorder

A randomized trial of the effect of escitalopram versus placebo on cognitive function in healthy first-degree relatives of patients with depression

Cognitive toxicity: from pesticides to pharmaceuticals

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