اثر درمانی اسیتالوپرام و ریبوکستین در اختلال عاطفی فصلی: تجزیه و تحلیل تجمع یافته

The monoaminergic neurotransmitters serotonin and noradrenaline have both been implicated in the pathogenesis of seasonal affective disorder (SAD). However, the differential therapeutic value of selective serotonin reuptake inhibitors (SSRI) and selective noradrenaline reuptake inhibitors (NARI) in SAD has not been assessed until now. This study compares data from two open-label trials with similar methodology investigating the SSRI escitalopram and the NARI reboxetine. 20 SAD patients were treated with escitalopram (10–20 mg) and 15 patients received treatment with reboxetine (fixed dosage: 8 mg) over 6 weeks. Ratings included the structured interview guide for the Hamilton depression rating scale, SAD version (SIGH–SAD), the clinical global impression of severity (CGI-S) and improvement (CGI-I) and the UKU side effect rating scale. Treatment led to a significant reduction in SIGH–SAD score, CGI-S and CGI-I after one week in the reboxetine group and after two weeks in the escitalopram group. SIGH–SAD score was significantly lower in the reboxetine group at weeks 1, 2 and 4 but not at the end of the study. The response rate (SIGH–SAD <50% of baseline value) and the remission rate (SIGH–SAD <8) were not significantly different after 6 weeks of treatment, but the time to response and to remission was significantly shorter in the reboxetine group. The number and severity of side effects were higher in patients treated with reboxetine at all time points. Thus escitalopram and reboxetine were equally effective in treating SAD on all primary and secondary outcome measures. Reboxetine displayed a faster onset of action, but was associated with more pronounced side effects. Further studies comparing SSRI and NARI in SAD are warranted.

Seasonal affective disorder (SAD) is a relatively frequent mood disorder in temperate climates. It is defined by reoccurence of depressive episodes in autumn and winter (fall-winter depression) alternating with remission or hypomania, more seldom mania, during the successive spring and summer (Rosenthal et al., 1984). Preliminary data indicate a high degree of social impairment and socioeconomic costs for patient suffering from SAD (Pjrek et al., 2008), highlighting the necessity of early recognition and adequate treatment. Bright light therapy is a first choice treatment for SAD patients (Winkler et al., 2006). However, light therapy is either not entirely effective or not suitable for other reasons in about 50% of cases (Pjrek et al., 2004). For those patients antidepressant drug treatment has been established as a viable alternative (Winkler et al., in press). Several studies have been conducted to elucidate the pathogenetic background of SAD: studies in drug-free patients employing monoamine depletion (Neumeister et al., 1998 and Stastny et al., 2003) and challenge tests (Coiro et al., 1993 and Schwartz et al., 1997), neuroimaging studies (Neumeister et al., 2001 and Willeit et al., 2000) and findings from studies exploring serotonin transporter function in SAD (Willeit et al., 2008) have suggested an involvement of the serotonergic, but also noradrenergic and dopaminergic neurotransmitter systems. However, the differential value and the specific clinical advantages and disadvantages of selectively influencing one of these monoaminergic neurotransmitters in the pharmacotherapy of SAD have not been assessed until now. The aim of this study was to compare existing data on treatment of SAD with escitalopram and reboxetine in regard to clinical efficacy and tolerability. Escitalopram is a selective serotonin reuptake inhibitor (SSRI) with high affinity to the serotonin transporter. It has been postulated that escitalopram binds to a secondary allosteric binding site on the serotonin transporter molecule, which is able to augment the efficacy of reuptake inhibition (Chen et al., 2005 and Klein et al., 2007). Reboxetine on the other hand is a potent and highly selective noradrenaline reuptake inhibitor (NARI), which is devoid of any relevant affinity to other neurotransmitter receptors (Kasper et al., 2000).