ریبوکستین در اختلال عاطفی فصلی: یک آزمایش باز
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|31769||2001||5 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : European Neuropsychopharmacology, Volume 11, Issue 1, February 2001, Pages 1–5
Seasonal affective disorder (SAD), winter type, is a condition characterized by the annual recurrence of depressive episodes during fall/winter, alternating with spring/summer euthymia or hypomania. Various neurotransmitters have been implicated in the etiology of SAD, the strongest evidence involving serotonin. Recently, increasing attention has been paid to the potential role of catecholaminergic pathways in the pathophysiology of SAD. We investigated the efficacy and tolerability of reboxetine, a selective noradrenaline inhibitor, in patients with SAD. Eleven out of sixteen patients who were included in a 6-week drug surveillance during winter season experienced full remission of depressive symptoms. Nine patients reported a rapid relief of preexistent severe atypical depressive symptoms within the first treatment week. Reboxetine might therefore be an effective and well-tolerated treatment option for SAD patients. In conclusion, our preliminary results are in line with evidence from recent studies suggesting that catecholaminergic systems might also be involved in the pathophysiology of SAD.
Seasonal affective disorder (SAD) is a condition characterized by annually occurring depressive episodes, the most usual pattern being symptom onset in fall and winter followed by full remission or hypomanic states during spring and summer (Rosenthal et al., 1984). Furthermore the optionally present so-called atypical depressive symptoms, e.g. hypersomnia, fatigue, hyperphagia, carbohydrate craving, and subsequent weight gain often precede impaired functioning (Tam et al., 1997). Emphasis has been put in evaluating treatment options for patients with SAD. The antidepressant effect of bright light therapy (BLT) in the treatment of seasonal depression is well documented (Eastman et al., 1998, Lewy et al., 1998 and Terman et al., 1998). In case patients do not respond sufficiently to light treatment or object to the usage of light therapy for logistical reasons, the best evidence so far for efficacy of antidepressants in SAD involve the selective serotonin reuptake inhibitors (SSRIs) with sertraline and fluoxetine having been studied predominantly (Lam et al., 1995, Blashko, 1995 and Kasper et al., 2000). Studying the biological basis of SAD, several studies focused on alterations in brain serotonergic systems (Wirz-Justice and Richter, 1979, Carlsson et al., 1980, Arora and Meltzer, 1988, Neumeister et al., 1997, Schwartz et al., 1997, Yatham et al., 1997, Neumeister et al., 2000a and Willeit et al., 2000). Little is known about the potential role of catecholaminergic pathways in the etiology of SAD. Evidence for the importance of catecholamines in the pathophysiology of SAD can be inferred from studies showing that (a) resting plasma norepinephrine levels are inversely correlated with the level of depression in drug-free SAD patients (Rudorfer et al., 1993), (b) BLT decreases the urinary output of norepinephrine and its metabolites (Anderson et al., 1992), (c) catecholamine depletion disrupts the beneficial effects of light therapy (Neumeister et al., 1998) and (d) dopamine transporter availability is reduced in untreated symptomatic depressed SAD patients (Neumeister et al., 2000b). In addition, mirtazapine, an antidepressant drug providing a dual mechanism by increasing noradrenergic and serotonergic neurotransmission, was found to be effective in a drug surveillance with patients suffering from SAD (Hesselmann et al., 1999). However, plasma concentrations of the major norepinephrine metabolite 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) did not differentiate depressed patients with SAD from controls or patients with SAD in BLT-induced remission, nor did cerebrospinal fluid levels in relation to either MHPG or the 5-HT metabolite 5-hydroxyindolaecetic acid (Rudorfer et al., 1993).