Journal of Psychosocial Nursing and Mental Health Services

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Psychopharmacology 

Somatic Therapies for Seasonal Affective Disorder

Robert H. Howland, MD

Abstract

The syndrome of seasonal affective disorder (SAD) is defined as a history of major depressive episodes that recur regularly at a particular time of year, typically fall or winter, and completely remit in the spring. It has been hypothesized that photoperiod-related changes in the duration of melatonin secretion may be involved in the seasonal mood cycles of SAD in human beings, suggesting that artificial bright lights (mimicking daylight) might be used to treat SAD. This article reviews studies on the use of bright light therapy and antidepressant medication for the treatment of SAD. Studies have found that bright light therapy and antidepressant medication are both effective for the treatment of SAD. Bright light therapy may also be effective for treating nonseasonal depression.

Abstract

The syndrome of seasonal affective disorder (SAD) is defined as a history of major depressive episodes that recur regularly at a particular time of year, typically fall or winter, and completely remit in the spring. It has been hypothesized that photoperiod-related changes in the duration of melatonin secretion may be involved in the seasonal mood cycles of SAD in human beings, suggesting that artificial bright lights (mimicking daylight) might be used to treat SAD. This article reviews studies on the use of bright light therapy and antidepressant medication for the treatment of SAD. Studies have found that bright light therapy and antidepressant medication are both effective for the treatment of SAD. Bright light therapy may also be effective for treating nonseasonal depression.

Dr. Howland is Associate Professor of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania.

The author discloses that he has no significant financial interests in any product or class of products discussed directly or indirectly in this activity, including research support.

Address correspondence to Robert H. Howland, MD, Associate Professor of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, 3811 O’Hara Street, Pittsburgh, PA 15213; e-mail: HowlandRH@upmc.edu.

The syndrome of seasonal affective disorder (SAD) was first described in 1984 (Rosenthal et al., 1984). SAD is defined as a history of major depressive episodes that recur regularly at a particular time of year, typically fall or winter, and completely remit in the spring. Patients with bipolar disorder or recurrent major depression are diagnosed as having SAD if they have had at least 2 years of seasonal depressive episodes. In addition, their seasonal depressive episodes must substantially outnumber any nonseasonal ones.

The photoperiod (duration of daylight) can be experimentally controlled in animal studies. Photoperiod-induced changes in the duration of nighttime melatonin secretion have been found to cause changes in various behaviors and functions. It has been hypothesized that similar photoperiod-related changes in the duration of melatonin secretion may be similarly involved in the seasonal mood cycles of SAD in human beings (Sohn & Lam, 2005). These findings have suggested that artificial bright lights (mimicking daylight) might be used to treat SAD.

Bright Light Therapy for SAD

In their seminal report describing SAD, Rosenthal et al. (1984) also presented their positive preliminary findings from the first controlled trial of bright light therapy. The original treatment protocol used a light intensity of 2,500 lux, given in 3-hour morning and evening sessions. Light therapy studies after this report investigated various treatment parameters, such as the exposure schedule, duration of exposure, and light intensity. In a review of 25 studies conducted during the 1980s, Terman et al. (1989) examined many of these treatment parameters. They found that 1 week of morning treatment produced a significantly higher remission rate (53%) compared with evening (38%) or midday (32%) treatment. Twice daily sessions were no more effective than morning sessions alone. Bright light treatment at morning, midday, and evening times was more effective than dim light controls (400 lux or less). Two-hour morning and 2-hour morning plus evening sessions were superior to brief light sessions (30 minutes).

More recently, Golden et al. (2005) reviewed randomized controlled trials of light therapy for seasonal and nonseasonal mood disorders. Bright light treatment and dawn simulation treatment were each effective in SAD. The dawn simulation studies used increasing light exposure from 0 lux to 200 to 300 lux over 1 to 2.5 hours starting before dawn. The dawn placebo condition consisted of an increase that was less than 5 lux and/or was less than 15 minutes in duration. Bright light treatment alone also was effective for nonseasonal depression, but light therapy as an adjunct to antidepressant medication was ineffective for non-seasonal depression. Two studies using a higher light intensity (10,000 lux) in brief (30-minute to 40-minute) sessions resulted in remission rates that were significantly greater than brief dim light (400 lux) and brief lower-level (3,000 lux) sessions (Magnússon & Kristbjarnarson, 1991; Terman et al., 1990).

Swedo et al. (1997) conducted a double-blind, placebo-controlled, crossover trial of bright light treatment in 28 children (ages 7 to 17). Patients entered a 1-week baseline period during which they wore dark glasses for an hour daily and were then randomly assigned to receive either active treatment or placebo for 1 week. Active treatment consisted of 2 hours of dawn simulation (to a maximum of 250 lux) plus 1 hour of bright light therapy (2,500 lux for patients younger than 9; 10,000 lux for those 9 and older) between 4 p.m. and 8 p.m. The placebo condition was 1 hour of clear goggles plus 5 minutes of low-intensity dawn simulation. After this phase, patients wore dark glasses again for 1 to 2 weeks and then were given the alternate treatment. Light therapy was significantly more effective than placebo.

Antidepressant Drug Therapy for SAD

Lingjaerde et al. (1993) investigated the efficacy of moclobemide (a selective, reversible inhibitor of monoamine oxidase A not currently available in the United States) 400 mg per day in a 14-day, double-blind placebo-controlled trial involving 34 patients. At endpoint, there were no statistically significant differences between the groups.

In a 5-week placebo-controlled study of 68 patients, Lam et al. (1995) investigated the efficacy of fluoxetine (Prozac®) 20 mg per day. Total depression scores at endpoint were lower in the fluoxetine group, but the difference was not statistically significant. The fluoxetine response rate (59%) was superior to the placebo response rate (34%). More severely depressed patients also responded better to drug than to placebo.

Partonen and Lönnqvist (1996) analyzed the outcome of a subgroup of 32 SAD patients who were among 183 depressed patients enrolled in a 6-week double-blind study comparing moclobemide 300 to 450 mg per day and fluoxetine 20 to 40 mg per day. There was no significant difference in outcome between moclobemide-treated or fluoxetine-treated SAD patients.

In an 8-week, double-blind placebo-controlled trial involving 178 patients, Moscovitch et al. (2004) found that sertraline (Zoloft®) 50 to 200 mg per day was significantly more effective than placebo. In addition, Martiny et al. (2004) investigated citalopram (Celexa®) for the continuation treatment of SAD in a large placebo-controlled study. After 1 week of successful bright light therapy, patients were randomized to citalopram 20 to 60 mg per day or placebo for 15 weeks. Citalopram was superior to placebo in preventing relapse.

Modell et al. (2005) described the findings from three prospective, randomized, placebo-controlled prevention trials that involved 1,042 nondepressed patients with a history of SAD. They were enrolled in autumn and treated until spring with bupropion XL (Wellbutrin® XL) 150 to 300 mg per day or placebo. Patients had an average of 13 previous seasonal depressive episodes. Major depression recurrence rates during the three studies were 19% versus 30%, 13% versus 21%, and 16% versus 31% (for bupropion XL versus placebo, respectively). Bupropion XL was significantly better than placebo for preventing the recurrence of seasonal major depressive episodes.

Light Therapy Versus Antidepressant Drug Therapy for SAD

Ruhrmann et al. (1998) conducted a randomized, double-blind study involving 40 patients. One week of placebo was followed by 5 weeks of treatment with fluoxetine (20 mg per day) plus a placebo light condition versus bright light (3,000 lux, 2 hours per day) plus a placebo drug. Response rates for light (70%) and fluoxetine (65%) were not significantly different. Remission rates for light (50%) were nonsignificantly higher than for fluoxetine (25%). Light therapy improved depression scores significantly faster compared with fluoxetine.

Lam et al. (2006) conducted a double-blind, randomized, controlled trial over three winter seasons in 96 patients. Patients were randomly assigned to 8 weeks of double-blind treatment with either 10,000-lux light treatment plus placebo capsule or 100-lux light treatment plus fluoxetine 20 mg per day. Light treatment was applied for 30 minutes per day in the morning. There were no significant differences in response or remission rates between treatments.

Clinical Use of Light Therapy

The general findings from clinical trials of light therapy suggest that patients with SAD are most likely to benefit from morning light administered shortly after awakening (Terman & Terman, 2005). The dosage of 10,000 lux for 30 minutes is most effective and most practical. Although lower intensities (e.g., 2,500 lux) can be effective, they require longer exposure durations of 2 to 3 hours. This may not be feasible for long-term daily use.

In addition to light intensity, another important factor is the wavelength spectrum of the light source. Ultraviolet (UV) and infrared (IR) wavelengths are potentially damaging to the eye. Because the light from incandescent lamps contains a very high amount of IR wavelengths, they should not be used. Hence, broad-spectrum white light from fluorescent lamps, in which UV and IR wavelengths have been filtered out, is considered effective and relatively safe.

Many commercial light boxes are available for the treatment of SAD, but they are not highly regulated. As a result, their efficacy and safety are not readily apparent. Although prescriptions are not needed, the selection and use of a commercial light box should be done only in consultation with a clinician who is very familiar with their technical requirements and clinical use. This will help ensure they are used most effectively and safely.

The patient is typically instructed to sit within several yards of the light box for each session. Patients can read or be involved in other activities, while glancing at the light box periodically. They do not need to stare at the light to achieve any benefit. Light therapy is given for a period of several days to weeks, until a satisfactory response is attained. Treatment can be repeated for depressive relapses. Side effects include eyestrain, headache, irritability, agitation, nausea, fatigue, and insomnia. Like antidepressant drugs, light therapy can trigger hypomania or mania. Patients receiving light therapy should be clinically monitored as closely as with other treatments.

Conclusion

Bright light therapy is effective for the treatment of SAD. If light therapy alone is not fully effective, some patients may benefit from switching to anti-depressant medication alone or by combining medication with light therapy. Nurses should be familiar with the use of light therapy, including possible side effects, as well as understand the particular treatment parameters that are most likely to be effective and safe.

References

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Authors

Dr. Howland is Associate Professor of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania.

Address correspondence to Robert H. Howland, MD, Associate Professor of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, 3811 O’Hara Street, Pittsburgh, PA 15213; e-mail: .HowlandRH@upmc.edu

10.3928/02793695-20090101-07

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