The Diagnostic and Statistical Manual of Mental Disorders, 4th ed., (DSM-IV) categorizes seasonal affective disorder (SAD) not as a unique mood disorder, but as a specifier of major depression.1 Thus, patients with SAD experience episodes of major depression that tend to recur at specific times of the year. These seasonal episodes may take the form of major depressive or bipolar disorders. Table 11 lists the DSM-IV criteria for the seasonal pattern specifier.
|Standardized screening instruments for SAD probably are not sensitive enough to be used for routine screening.
|Light therapy may be used for treating SAD, with effect sizes similar to those for antidepressant medications in treating depression. The total daily dosage should be approximately 5,000 lux, administered in the morning over 30 to 120 minutes.
|Cognitive behavior therapy may be considered as an alternative to light therapy in the treatment of SAD.
The overall lifetime prevalence of SAD ranges from 0 to 9.7 percent.2 This estimate depends on the specific population studied, as well as whether SAD is diagnosed by a screening questionnaire or a more rigorous clinical interview. In one U.S. study that used DSM-IV–based criteria, the lifetime prevalence of major depression with a seasonal pattern was 0.4 percent.3 Prevalence may be higher at northern latitudes, and it may vary within ethnic groups at the same latitude.4
Patients with SAD are more likely to have family members with SAD, although this may be subject to reporting bias.5 Twin studies have found that there may be a genetic component to susceptibility. Several genes code for serotonin transport, but the overall pattern of heritability likely is complex and polygenomic.6
Patients with SAD have more outpatient visits, more diagnostic testing, more prescriptions, and more referrals throughout the year compared with age- and sex-matched controls.7 Patients with SAD visit their primary care physician more often in the winter than other patients, but rates between the groups are similar the rest of the year.8
Screening for SAD
Primary care physicians routinely fail to diagnose nearly one half of all patients who present with depression and other mental health problems.9 Because SAD is a subtype of major depression, screening for depression should theoretically help identify patients with this disorder. The U.S. Preventive Services Task Force (USPSTF) concluded that there is good evidence that screening improves the accurate identification of patients with depression in primary care settings, and that treatment decreases clinical morbidity. The USPSTF concluded that the benefits of screening likely outweigh any potential harms.10
There are several instruments for detecting depression in primary care, ranging in length from one to 30 items with an average administration time of two to six minutes. Typically, the reading level of these instruments is between the third- and fifth-grade levels.11 Some standardized instruments focus more narrowly on SAD. Reports on the sensitivity and specificity of these instruments can be difficult to interpret because of the small sizes and heterogeneity of patient samples tested, the possibility of differential recall bias (depending on the time of year the test is administered), and ongoing controversy over the criteria standard for SAD.
The Seasonal Pattern Assessment Questionnaire (SPAQ) is perhaps the most widely studied tool. It has been reported to have a high specificity (94 percent) for SAD but a low sensitivity (41 percent).12 Other authors, however, have reported a much lower specificity.13 The Seasonal Health Questionnaire has been reported to have higher specificity and sensitivity than the SPAQ,14 but these results must be confirmed in larger and more diverse patient groups.
Although benefits from screening are less likely to be achieved without an accurate diagnostic work-up, effective treatment interventions, and close follow-up, it is unclear whether screening ultimately improves the care and outcomes of patients with major depression. When deciding to implement a screening instrument in a practice, office personnel should consider the administration time, scoring ease, reading level, and usefulness in identifying major depression and assessing change in the depression scores over time.15
Once patients have been identified as having major depression, questions must be asked to determine if the depression is linked to SAD. These questions concern the relationship between depression and time of year (if remission occurs during certain times of the year) and whether the depression has occurred at the same time during the past two years.
Because SAD is associated with serotonergic dysregulation and possibly with noradrenergic mechanisms, it may overlap with other diagnoses that share similar mechanisms, including generalized anxiety disorder, panic disorder, bulimia nervosa, late luteal phase dysphoric disorder, and chronic fatigue syndrome.16 SAD also may be associated with attention-deficit/hyperactivity disorder (ADHD). Both conditions have been described as “disorders of central under-arousal coupled with a heightened sensitivity to stimuli from the physical environment,” and both are more common in women with a particular genotype for HTR2A, a gene that codes for a serotonin receptor.17,18
A pattern of seasonal alcohol use also may be associated with SAD. A summary of current research findings concluded that some patients with alcoholism may be self-medicating an underlying depression with alcohol or manifesting a seasonal pattern to alcohol-induced depression.19 Such patterns appear to have a familial component and, like the link between ADHD and SAD, may be related to serotonergic functioning.
Treatment options for SAD include light therapy, cognitive behavior therapy, and pharmacotherapy. Each option has been proven beneficial in treating SAD, but no large studies have found any treatment to be superior.
Among susceptible persons, decreased seasonal exposure to light may mediate SAD through phase shifts in circadian rhythms, with resulting alterations in several aspects of serotonin metabolism. Thus, light replacement has been the most widely studied treatment for SAD.20 In a review of studies of light therapy, an average dosage of 2,500 lux daily for one week was superior to placebo, as indicated by improvements on a depression rating scale.21 The dosage most often found to be effective is 5,000 lux per day, given as 2,500 lux for two hours or 10,000 lux for 30 minutes.22 A recent meta-analysis of 23 studies of light therapy found that the odds ratio for remission was 2.9 (95% confidence interval, 1.6 to 5.4); this ratio is similar to those of many pharmaceutical treatments for depression.23 Like drug therapy for depression, light therapy carries some risk of precipitating mania.24
To ensure adequate response, patients should be treated with light therapy units that are specifically designed to treat SAD. Units that are not specifically designed for SAD treatment may not provide adequate brightness and may not have appropriate ultraviolet light filtration.22
COGNITIVE BEHAVIOR THERAPY
Although cognitive behavior therapy (CBT) has some effectiveness in improving dysfunctional automatic thoughts and attitudes, behavior withdrawal, low rates of positive reinforcement, and ruminations in patients with major depression, few studies have assessed its effectiveness in the treatment of SAD. In one small clinical trial, patients with SAD were randomized to six weeks of treatment with CBT or light therapy, or CBT plus light therapy.28 At the end of treatment, all three groups had significantly decreased levels of depression, but there was no difference between groups. However, this study only enrolled 26 subjects. To date, there have been no studies large enough to establish the effectiveness of CBT in the treatment of SAD.
Because patients with SAD also must fulfill criteria for depression, several randomized trials have assessed the use of antidepressants for this condition.29–33 Most of these studies have compared pharmacotherapy with placebo rather than light therapy, making it difficult to determine if one treatment is superior. In the largest of these trials, patients with SAD had significantly better response on several measures of depression after eight weeks of sertraline (Zoloft) therapy compared with control patients.29 Patients were excluded if they were receiving light therapy or other psychoactive medications, or if they had a history of alcoholism, drug abuse, or “emotional or intellectual problems.”
A smaller study found that, in some statistical analyses, fluoxetine (Prozac) was better than placebo in the treatment of SAD.30 Another small study found that the monoamine oxidase inhibitor moclobemide (not available in the United States) was similar to placebo in terms of changes on several general depression scales.31
Few randomized trials have assessed the effect of light therapy compared with pharmacotherapy.32,36 These trials failed to find a difference between the effect of 6,000 lux and that of 20 mg of fluoxetine daily,32 or between 10,000 lux and 20 mg of fluoxetine daily.36 Larger trials will be required to establish whether there is a difference in effect size between light therapy and pharmacotherapy.
It is also possible that pharmacotherapy may preserve an initial therapeutic response to light therapy. Among 168 patients who had a positive response to light therapy, citalopram (Celexa) was found to be no more effective than placebo at preventing relapse; however, it was superior in terms of some secondary measures of depression.33 In general, current evidence does not provide clear guidance as to whether antidepressant treatment is superior to light therapy, or whether antidepressants are useful as an adjunct to light therapy.