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Seasonal affective disorders.

Seasonal affective disorder is a pattern of major depressive episodes that occur and remit with changes in seasons. It may be seen in major depressive or bipolar disorders, as described in the Diagnostic and Statistical. Manual of Mental Disorders (DSM-IV). The most recognized form of seasonal affective disorder, "winter depression," is characterized by recurrent episodes of depression, hypersomnia, augmented appetite with carbohydrate craving, and weight gain that begin in the autumn and continue through the winter months. Physicians have many options for treating seasonal affective disorder. While questions regarding the validity of seasonal affective disorder as a syndrome and the mechanism of action of light therapy continue to be investigated, the established effectiveness of light therapy in patients with winter depression supports the usefulness of assessment for this seasonal pattern and consideration of light therapy as an option in addition to existing treatment choices.

Diagnosis, Differential↗

Pharmacotherapy of seasonal affective disorder.

Seasonal affective disorder is a common variant of recurrent major depressive disorder or bipolar disorder. Treatment with bright artificial light has been found to be effective in this condition. However, for patients who do not respond to light therapy or those who lack compliance, conventional drug treatment with antidepressants also has been proposed. Substances with selective serotonergic or noradrenergic mechanisms should be preferred over older antidepressants. Although there are a number of open and controlled studies evaluating different compounds, these studies were often limited by relatively small sample sizes. Furthermore, there are no studies specifically addressing bipolar seasonal depression. This article will review the published literature on pharmacotherapy of seasonal affective disorder.

Dopamine Agonists↗

Hypericum in the treatment of seasonal affective disorders.

Seasonal affective disorder (SAD) represents a subgroup of major depression with a regular occurrence of symptoms in autumn/winter and full remission in spring/summer. Light therapy (LT) has become the standard treatment of this type of depression. Apart from this, pharmacotherapy with antidepressants also seems to provide an improvement of SAD symptoms. The aim of this controlled, single-blind study was to evaluate if hypericum, a plant extract, could be beneficial in treating SAD patients and whether the combination with LT would be additionally advantageous. Patients who fulfilled DSM-III-R criteria for major depression with seasonal pattern were randomized in a 4-week treatment study with 900 mg of hypericum per day combined with either bright (3000 lux, n = 10) or dim (< 300 lux, n = 10) light condition. Light therapy was applied for 2 hours daily. We found a significant (MANOVA, P < .001) reduction of the Hamilton Depression Scale score in both groups but no significant difference between the two groups. Our data suggest that pharmacologic treatment with hypericum may be an efficient therapy in patients with seasonal affective disorder.

Adult↗

Seasonal affective disorder.

Seasonal affective disorder (SAD) is a form of recurrent depressive or bipolar disorder, with episodes that vary in severity. Seasonal patterns of depressive episodes are common, but SAD seems to be less common than such patterns suggest. SAD was at first believed to be related to abnormal melatonin metabolism, but later findings did not support this hypothesis. Studies of brain serotonin function support the hypothesis of disturbed activity. The short-allele polymorphism for serotonin transporter is more common in patients with SAD than in healthy people. Atypical depressive symptoms commonly precede impaired functioning, and somatic symptoms are frequently the presenting complaint at visits to family physicians. The best treatment regimens include 2500 Ix of artificial light exposure in the morning. When patients seem to have no response or to prefer another treatment, antidepressants should be considered.

Brain↗

Rhythm and blues: the theory and treatment of seasonal affective disorder.

Seasonal affective disorder (SAD) is a depressive disorder which occurs during the winter and remits in the spring and summer. It differs from non-seasonal depression in its seasonal variation and in the presence of neurovegetative symptoms such as increased appetite and hypersomnia. This review is aimed at clinical practitioners and presents a detailed description of the syndrome before discussing the assessment of SAD and the current treatment of choice of phototherapy. Particular attention is paid to the impotant issue of differential diagnosis during assessment and the practicalities involved in the administration of light therapy during treatment.

Adult↗

Open study of effects of alprazolam on seasonal affective disorder.

Seasonal affective disorder (SAD) differs from depression with melancholic features in atypical symptoms, such as hyperphagia, hypersomnia and weight gain. Moreover, SAD is confined to a certain season of the year. We examined the pharmacological efficacy of alprazolam for treatment of patients with SAD. Six patients with SAD were treated with alprazolam at doses of 1.2 mg/day or 1.2 mg/day first and then 2.4 mg/day for 2 weeks. The improvement was evaluated by the change of total score of the SIGH-SAD (with both 21 items HAMD and eight items atypical symptoms) and the clinical global impression (CGI). Although only two patients showed a remarkable improvement by SIGH-SAD, all patients showed a higher than moderate improvement with CGI. Our findings suggest that alprazolam might be efficacious for certain SAD patients.

Adolescent↗

Treatment of seasonal affective disorder.

Seasonal affective disorder (SAD), winter type, is characterized by the regular annual onset of major depressive episodes during fall or winter, followed by spontaneous remission and sometimes hypomanic or manic episodes during spring and summer. SAD is clinically important, since approximately 2-5% of the general population in temperate climates are affected. Since the first description of the syndrome, researchers have made attempts to elucidate the pathophysiological background of SAD. Bright light therapy has been proposed as the treatment of choice for this disorder. However, numerous studies have also investigated suitable psychopharmacological treatments for SAD. This report is aimed to provide an overview on the clinical management and current therapeutic options for SAD.

Behavior Therapy↗

Vitamin D vs broad spectrum phototherapy in the treatment of seasonal affective disorder.

Seasonal Affective Disorder (SAD) is prevalent when vitamin D stores are typically low. Broad-spectrum light therapy includes wavelengths between 280-320 nm which allow the skin to produce vitamin D. This study was designed to test the hypothesis that vitamin D deficiency might play a role in SAD. A prospective, randomized controlled trial was conducted in a group of 15 subjects with SAD. Eight subjects received 100,000 I.U. of vitamin D and seven subjects received phototherapy. At the onset of treatment and after 1 month of therapy subjects were administered the Hamilton Depression scale, the SIGH-SAD, and the SAD-8 depression scale. All subjects also had serum levels of 25-hydroxyvitamin D (25-OH D) measured before and 1 week after intervention therapy. All subjects receiving vitamin D improved in all outcome measures. The phototherapy group showed no significant change in depression scale measures. Vitamin D status improved in both groups (74% vitamin D group, p < 0.005 and 36% phototherapy group, p < 0.01). Improvement in 25-OH D was significantly associated with improvement in depression scale scores (r2=0.26; p=0.05). Vitamin D may be an important treatment for SAD. Further studies will be necessary to confirm these findings.

Adolescent↗

Seasonal affective disorders.

Seasonal affective disorders is a form of recurrent depression that appears to be precipitated by a specific stressor (i.e., winter) and resolves spontaneously in spring or summer. The elements of winter that must contribute to SAD are unknown at this time although light deficiency most likely plays a role. It is similar to late luteal dysphoric disorder because of the circumscribed time course, range of severity and female predominance. Atypical anergic symptoms usually dominate the clinical picture but more typical anxious and agitated symptoms can be present. Onset and offset of symptoms and severity varies greatly. Fall onset is usually gradual while spring remission can be more startling and abrupt producing hypomania in some patients. Full summer remission occurs in most patients when followed prospectively and is associated with improvement in personality and biological measures. Most patients improve with light therapy but it is not known how sustained this effect is or whether it is comparable to treatment with antidepressants in similarly affected patients. BL treatment also implies a single etiological mechanism of SAD, but this is still unproven. Lights, while effective do not appear to be as effective as summer. This could be because most BL clinical trials have been too brief to actually simulate summer or because of the significant heterogeneity in population. It is important to remember that lights alone cannot replicate summer conditions. Summer light is up to ten times stronger than currently available light boxes and the season produces many other environmental and social changes. Most likely SAD will prove similar to other forms of depression in that it is a multidimensional problem which requires a variety of treatments to alleviate various aspects of the syndrome.

Antidepressive Agents↗

2- versus 4-hour evening phototherapy of seasonal affective disorder.

Seasonal affective disorder (SAD) has been successfully treated with bright light, and morning exposure has been deemed more effective than exposure at other times. Evening treatment may offer a practical advantage, but the optimal duration of exposure has not been established. Six SAD patients were treated at home for 1 week with 2500 lux of light given either from 6 p.m. to 8 p.m. or from 6 p.m. to 10 p.m. using a counterbalanced crossover design with a minimal withdrawal period of 1 week between conditions. Both treatments were effective in reversing SAD symptoms, but neither treatment was superior. These results suggest that evening phototherapy for as little as 2 hours may be a useful and reasonable alternative for the treatment of SAD.

Adult↗

Monoaminergic function in the pathogenesis of seasonal affective disorder.

Seasonal affective disorder/winter type (SAD) is characterized by recurrent depressive episodes during autumn and winter alternating with non-depressive episodes during spring and summer. Light therapy with full-spectrum, bright white light has been shown to be effective for this condition. Several hypotheses have been discussed in the literature about the pathogenesis of SAD. The most prominent includes disturbances in central monoaminergic transmission. Evidence can be inferred from studies showing a seasonal rhythm of central and peripheral serotonergic functioning which may be a predisposing factor for SAD. Some of the symptoms of SAD are believed to represent an attempt to overcome a putative deficit in brain serotonergic transmission. Moreover, 5-HT receptor challenge studies suggest altered activity at or downstream to central 5-HT receptors. Monoamine depletion studies support hypotheses about serotonergic and catecholaminergic dysfunctions in SAD and suggest that light therapy may well compensate for this underlying deficit. Further, albeit indirect, support for the importance of monoaminergic mechanisms in SAD and its involvement in the mechanism of the action of light therapy comes from studies showing antidepressant efficacy of serotonergic and noradrenergic antidepressants in the treatment of SAD. Altogether, disturbances in brain monoaminergic transmission seem to play a key role in the pathogenesis of SAD; monoaminergic systems may also play an important role in the mechanisms of the action of light therapy.

Biogenic Monoamines↗

Role of serotonin transporter promoter repeat length polymorphism (5-HTTLPR) in seasonality and seasonal affective disorder.

Seasonal variations in mood and behavior (seasonality) and seasonal affective disorder (SAD) have been attributed to seasonal fluctuations in brain serotonin (5-HT). the short (s), as opposed to the long (l), allele of the 5-HT transporter linked polymorphism (5-HTTLPR) has been associated with neuroticism and depression. We hypothesized that this short allele would also be associated with SAD and with higher levels of seasonality. Ninety-seven SAD patients and 71 non-seasonal healthy controls with low seasonality levels were genotyped for 5-HTTLPR and compared statistically. Patients with SAD were less likely to have the l/l genotype (27.8% vs 47.9%; P < 0.01) and more likely to have the s allele (44.8% vs 32.4%; P < 0.02) as compared to controls. The three 5-HTTLPR genotypes were also differentially distributed in patients and controls (P < 0.03). The SAD patients with the l/l genotype had a lower mean seasonality score than did patients with the other two genotypes (mean +/- s.d. = 15.3 +/- 2.8 vs 17.1 +/- 3.4 respectively; P < 0.02). The 5-HTTLPR short allele contributes to the trait of seasonality and is a risk factor for SAD, providing further evidence for a relationship between genetic variation in the 5-HT transporter (5-HTT) and behavior.

Affect↗

Alcoholism and seasonal affective disorder.

Seasonal changes in mood and behavior (seasonality) may be closely related to alcoholism. Some patients with alcoholism have a seasonal pattern to their alcohol misuse. They may be self-medicating an underlying seasonal affective disorder (SAD) with alcohol or manifesting a seasonal pattern to alcohol-induced depression. Both genetic and environmental factors play a role in the etiology and pathogenesis of alcoholism and SAD, operating, at least in part, through the brain serotonergic system. Family and molecular genetic studies suggest that there may be a genetic link between seasonality and alcoholism. Certain environmental and social factors may contribute to the development of seasonality in patients with alcoholism. The fact that SAD and alcoholism may be comorbid shows the importance of a thorough diagnostic interview. Both mental health and drug and alcohol professionals should be provided with education to assist with appropriate identification, management, and referral of patients presenting with comorbid alcoholism and SAD.

Alcoholism↗

Genetic studies of seasonal affective disorder and seasonality.

Genetic studies of seasonal affective disorder (SAD) and seasonality have received considerable attention over the past several years. Studies of the prevalence of SAD and nonseasonal mood disorders among relatives of patients with SAD suggested a familial contribution to the development of SAD. Two twin studies demonstrated a substantial role of genetic variation in seasonality. Two genetic variants related to serotonergic transmission, the 5-HTTLPR and the 5-HT(2A)-1438G/A gene promoter polymorphisms, have been found to be associated with SAD. 5-HTTLPR is also associated with seasonality in SAD patients and in the general population. It is not clear whether SAD is inherited as a distinct entity or whether seasonality and depression are separate heritable traits that happen to coincide in certain individuals. Vulnerability to SAD and disease pathology may be influenced by many genes, perhaps on several chromosomes.

Dopamine↗

The role of genetic factors in the etiology of seasonal affective disorder and seasonality.

The study of the genetic basis of seasonal affective disorder (SAD), a condition where depressions in fall and winter alternate with nondepressed periods in the spring and summer, has recently received attention. The data on the genetics of seasonal affective disorders are of three types: 1. Familiality: Studies on the prevalence of psychiatric disorders among relatives of patients with SAD suggested a familial contribution to the development of SAD; 2. Heritability: A survey of a cohort of twins showed that genetic effects exert a global influence across a variety of behavioral traits and accounted for at least 29% of the variance in seasonality in men and women; 3. Molecular genetic research: two genetic variants related to serotonergic transmission, the 5-HTTLPR and the 5-HT2A-1438G/A gene promoter polymorphisms, are associated with SAD; the former but not the latter polymorphism is related to seasonality. Future research may clarify the role of different genes in the development of SAD.

Adult↗

A placebo-controlled study of sertraline in the treatment of outpatients with seasonal affective disorder.

RATIONALE: Seasonal affective disorder (SAD) is a relatively common cyclical depressive illness characterized by seasonal depressions during winter. The disorder is commonly responsive to light therapy, but antidepressant drug efficacy has not been definitely established. Serotonin selective re-uptake inhibitors are potentially efficacious treatments for SAD. OBJECTIVES: The objective of this study was to evaluate the efficacy, tolerability and safety of sertraline treatment for SAD. METHODS: One hundred and eighty seven outpatients with seasonal pattern recurrent winter depression (DSM-III-R defined) and a minimum 29-item Hamilton depression scale (SIGH-SAD version) score of 22 were randomized to 8 weeks treatment with either sertraline or placebo in a double-blind, multi-country, multi-center, parallel-group, flexible dose (50-200 mg once daily) study. Efficacy was investigated using physician and patient-rated scales measuring depression, anxiety and symptoms characteristic of seasonal affective disorder. RESULTS: Sertraline produced a significantly greater response than placebo at endpoint as measured by changes in the 29-item and 21-item Hamilton depression scales, the clinical global impression (CGI) severity scale, the Hamilton anxiety scale, and the hospital anxiety and depression scale. The proportion of sertraline-treated subjects achieving a response on the CGI improvement rating (ratings of 1 or 2) at endpoint (last observation carried forward) was significantly greater than that of the placebo group. Overall sertraline was well tolerated with the most frequent placebo adjusted adverse events, being nausea, diarrhea, insomnia and dry mouth. Adverse events were mostly mild to moderate and transient. CONCLUSIONS: Sertraline pharmacotherapy has been demonstrated to be an effective and well-tolerated therapy for out patients with SAD. As such, sertraline offers an important pharmacological option in the clinical management of this condition.

Adolescent↗

DSM-III-R personality disorders in seasonal affective disorder: change associated with depression.

Forty-five patients with winter Seasonal Affective Disorder (SAD) completed the Personality Diagnostic Questionnaire-Revised (PDQ-R) in a depressed state before starting therapy (light or medication), and again 14 weeks later when the scores on the Montgomery Asberg Depression Rating Scale (MADRS) had been reduced by an average of 74%. Prevalence and pattern of personality disorders (PDs) before treatment were similar to that found in patients with nonseasonal major depressive disorder (MDD) during a depressive episode. Number of categorical diagnoses were lower at follow-up for most PDs, but differences were not statistically significant. However, for dimensional scores (number of positive DSM-III-R criteria) significant changes were found for schizotypal, histrionic, narcissistic, and obsessive-compulsive PD, and for total dimensional score in cluster B and total score for all PDs. These changes differ from findings in similar studies of outpatients with nonseasonal MDD. Whether this indicates a specific pattern of change for patients with SAD is discussed. Multiple regression analysis showed a significant association between changes in positive PD criteria between the depressed and nondepressed state and change in depression score. No significant relationship was found between changes in PD criteria and Global Seasonality Score (GSS), a measure reflecting the sum of ratings of seasonal variation in sleep length, social activity, mood, weight, appetite, and energy level.

Adult↗