Comparative effectiveness of second-generation antidepressants for accompanying anxiety, insomnia, and pain in depressed patients: A systematic review

Danube University Krems, Krems, Austria.
Depression and Anxiety (Impact Factor: 4.41). 06/2012; 29(6):495-505. DOI: 10.1002/da.21951
Source: PubMed


Patients with major depressive disorder (MDD) often suffer from accompanying symptoms that influence the choice of pharmacotherapy with second-generation antidepressants (SGAs). We conducted a systematic review to determine the comparative effectiveness of citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, desvenlafaxine, duloxetine, venlafaxine, bupropion, mirtazapine, nefazodone, and trazodone, for accompanying anxiety, insomnia, and pain in patients with MDD.
We conducted searches in multiple databases including MEDLINE®, Embase, the Cochrane Library, International Pharmaceutical Abstracts, and PsycINFO, from 1980 through August 2011 and reviewed reference lists of pertinent articles. We dually reviewed abstracts, full-text articles, and abstracted data. We included randomized, head-to-head trials of SGAs of at least 6 weeks' duration. We grouped SGAs into three classes for the analysis: selective serotonin reuptake inhibitors (SSRIs), serotonin norepinephrine reuptake inhibitors, and others. We graded the strength of the evidence as high, moderate, low, or very low based on the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group (GRADE) approach.
We located 19 head-to-head trials in total: 11 on anxiety, six on insomnia, and four on pain. For the majority of comparisons, the strength of the evidence was moderate or low: evidence is weakened by inconsistency and imprecision. For treating anxiety, insomnia, and pain moderate evidence suggests that the SSRIs do not differ.
Evidence guiding the selection of an SGA based on accompanying symptoms of depression is limited. Very few trials were designed and adequately powered to answer questions about accompanying symptoms; analyses were generally of subgroups in larger MDD trials.

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Available from: Erin E Krebs, Mar 23, 2015
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    • "The well documented mechanisms about the antidepression effects of ADs is the inhibition of the reuptake of neurotransmitters such as DA, NE, and 5-HT or inhibition of the catabolism of neurotransmitters [21,22]. The analgesic effect of ADs have well studied and reviewed previously [23]. The mechanisms of ADs for pain killing have not been well known yet. "
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    ABSTRACT: The chronic pain can disturb physical, psychological, and social performances. Analgesic agents are widely used but some antidepressants (ADs) showed analgesia also. Bupropion is using for smoke cessation but it can change morphine withdrawal signs such as pain. This study tested the acute systemic effect of bupropion on formalin induced pain behavior in rats. Wistar male healthy rats were divided into 7 groups (control, sham, and 5 treated groups with 10, 30, 90, 120, and 200 mg/kg of bupropion, i.p.). The bupropion injected 3 hours prior to formalin induced pain behavior. Formalin (50 µl, 2.5%) was injected subcutaneously in dorsal region of right hindpaw in all animals. Nociceptive signs were observed continuously on-line and off-line each minute. Common pain scoring was used for pain assessment. The analysis of data by one-way ANOVA showed that bupropion can reduce pain scores in the second phase but not in first phase. Bupropion decreased the licking/biting duration significantly in first and second phase of formalin test. The results showed that bupropion has analgesic effects at systemic application. The change of second phase of the pain behavior was significant and it revealed that central mechanisms involve in bupropion analgesia.
    The Korean journal of pain 04/2014; 27(2):118-24. DOI:10.3344/kjp.2014.27.2.118
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    • "been proved that memory processes were altered by the REM sleep deprivation (Martella et al. 2012). Citalopram, a selective serotonin reuptake inhibitor (SSRI) is widely prescribed in serotoninergic dysfunctions related disorder (Thaler et al. 2012). This drug has a negative impact on cognitive functions in humans and in animals (Almeida et al. 2009; Archer et al. 1984; Burghardt et al. 2004; Hashimoto et al. 2009; Majlessi and Naghdi 2002), but the mechanism of citalopram-induced cognitive impairments is unknown. "
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    ABSTRACT: Rapid eye movement (REM) sleep is known to be essential for memory. Hence, REM sleep deprivation impairs memory processes. The frequently prescribed selective serotonin reuptake inhibitors (SSRIs) are known to cause REM sleep deprivation and to impair cognitive performance in humans and rodents. We suggested that impaired memory processes by citalopram in C57/BL6 mice could be explained by the acute inhibition of REM sleep. We hypothesized that those acute citalopram 5 and 10 mg/kg injections induced REM sleep deprivation, altered cognitive performance in passive avoidance, impaired spatial memory compared to controls. Three experiments have been realized: (1) mice received successively physiological saline, injection of citalopram 5 and 10 mg/kg and were recorded by polysomnographic recording after each injection. (2) Cognitive performance was evaluated in the passive avoidance with two groups of mice. One group received citalopram before training and one, after training. (3) Spatial learning was evaluated with another group of animals in the Y-maze test. At 5 and 10 mg/kg, citalopram delayed REM sleep onset and decreased REM sleep amounts (vs. controls). The same doses were administrated in the passive avoidance test and have significantly shortened latency to enter the dark compartment. In the Y-maze, citalopram-treated mice showed a decreased percentage of time spent in the novel arm in contrast to the two other arms compared with controls. We showed that citalopram impaired cognitive performance in behavioral tasks. Those impairments could be linked to REM sleep deprivation induced by citalopram although causal relationship needs to be investigated in further studies.
    Journal of Neural Transmission 10/2012; 120(3). DOI:10.1007/s00702-012-0901-0 · 2.40 Impact Factor
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    ABSTRACT: The Brown Norway (BN; BN/NHsdMcwi) rat exhibits a deficit in ventilatory CO2 sensitivity and a modest serotonin (5-HT) deficiency. Here, we tested the hypothesis that the selective serotonin reuptake inhibitor fluoxetine would augment CO2 sensitivity in BN but not Sprague Dawley (SD) rats. Ventilation during room air or 7% CO2 exposure was measured before, during and after 3 weeks of daily injections of saline or fluoxetine (10mg/(kgday)) in adult male BN and SD rats. Fluoxetine had minimal effects on room air breathing in BN and SD rats (p>0.05), although tidal volume (VT) was reduced in BN rats (p<0.05). There were also minimal effects of fluoxetine on CO2 sensitivity in SD rats, but fluoxetine increased minute ventilation, breathing frequency and VT during hypercapnia in BN rats (p<0.05). The augmented CO2 response was reversible upon withdrawal of fluoxetine. Brain levels of biogenic amines were largely unaffected, but 5-HIAA and the ratio of 5-HIAA/5-HT were reduced (p<0.05) consistent with selective and effective 5-HT reuptake inhibition. Thus, fluoxetine increases ventilatory CO2 sensitivity in BN but not SD rats, further suggesting altered 5-HT system function may contribute to the inherently low CO2 sensitivity in the BN rat.
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