Cns drugs 2007; 21 (11): 901-909

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2007, Vol. 21, No. 11 (pp. 901-909)ISSN: 1172-7047 Therapy In PracticeLong-Term and Preventative Treatment for SAD Terms and Conditions for Use of PDF
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Long-Term and Preventative
Treatment for Seasonal
Affective Disorder
Asa Westrin1 and Raymond W. Lam2 1 Department of Clinical Sciences, Division of Psychiatry, Lund University Hospital, 2 Division of Clinical Neuroscience, Department of Psychiatry, University of British Columbia This material is
(UBC), Vancouver, British Columbia, Canada the copyright of the
Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9011. Longer Term Treatment Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9032. Maintenance and Prevention Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9033. Clinical Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9064. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 907 original publisher.
Recurrent major depressive disorder with regular seasonal patterns, commonly Unauthorised copying
known as seasonal affective disorder (SAD), has evoked substantial research inthe last two decades. It is now recognised that SAD is a common condition withprevalence rates between 0.4% and 2.9% of the general population, and thatpatients with SAD experience significant morbidity and impairment in psychoso-cial function.
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There is good evidence that bright light therapy and antidepressant medica- tions are effective for the short-term treatment of SAD; however, given that SADis characterised by recurrent major depressive episodes, long-term and mainte-nance treatment must be considered. Unfortunately, there are few studies of longerterm (>8 weeks) and maintenance (preventative) treatments for SAD. The weight is prohibited.
of evidence suggests that light therapy usually needs to be continued dailythroughout the winter season because of rapid relapse when light is stopped tooearly in the treatment period. However, some studies support the use ofantidepressants to continue the response from a brief (1–2 weeks) course of lighttherapy early in the depressive episode, as soon as the first symptoms emerge inautumn. Only small studies have examined preventative treatment (before onset ofsymptoms) with light therapy, all of which have methodological limitations. Thebest evidence for preventative treatment in SAD comes from antidepressantstudies. Three large, randomised, placebo-controlled studies have shown thatpreventative treatment with bupropion XL reduces the recurrence rate of depres-sive episodes in patients with SAD.
Given the limitations in the evidence base and the inconsistent recurrence rate of winter depressive episodes, clinical recommendations for long-term and pre-ventative treatment must individualise treatment choices and weigh potentialbenefits against possible adverse effects.
The DSM-IV describes seasonal affective disor- antidepressant medications.[14] Despite some meth- der (SAD) as “recurrent major depressive episodes odological issues in designing appropriate placebo with regular seasonal patterns”.[1] Such episodes conditions, several systematic reviews and meta- occur most commonly during autumn and winter, analyses have shown that light therapy is an effec- and remit (or switch to hypomania or mania) during tive short-term treatment for SAD.[15,16] The most spring and summer.[2] Some patients with SAD may recent meta-analysis found a large effect size of 0.84 This material is
experience nonseasonal depressive episodes during (95% CI 0.6, 1.08) for bright light therapy compared their lifetime, but these are substantially less fre- with control conditions.[16] Similarly, while there are quent than the seasonal episodes. SAD is also asso- fewer studies of antidepressants in the short-term ciated with so-called atypical depressive symptoms, treatment of SAD, randomised controlled trials including hypersomnia, increased appetite and eat- the copyright of the
(RCTs) of SSRIs, such as fluoxetine (20 mg/day)[17] ing, carbohydrate craving and weight gain.[3] and sertraline (50–200 mg/day),[18] have shown evi- SAD is a relatively common condition. Epidemi- dence for efficacy in this disorder. Comparative ological studies, based on diagnostic interviews and studies and smaller, open-label studies suggest that DSM criteria, found prevalence rates for this disor- other antidepressants, such as bupropion, reboxetine original publisher.
der in the general population of 0.4% in the US[4] and moclobemide, may also be effective.[19-22] A and 1.7–2.9% in Canada.[5,6] Other studies, using direct comparison study has shown that light therapy self-report questionnaires, have shown community and fluoxetine have similar effectiveness in SAD,[23] prevalence rates for SAD ranging from <1% to but unfortunately there are no studies of combina- >10%.[3] The aetiology of SAD remains unknown, Unauthorised copying
tion light and medication treatment.
but major theories of the pathophysiology of this These studies have all addressed the short-term disorder include circadian hypotheses, neurotrans- treatment of SAD.[15-23] In the management of de- mitter dysfunction hypotheses and genetic hypothe- pression, we now recognise that there are also con- tinuation and/or maintenance phases of treatment in and distribution
The depressive symptoms in SAD result in sig- which the objectives of care are to prevent relapse nificant morbidity and impairment in psychosocial and recurrence.[24,25] In fact, most clinical practice function. Patients with seasonal depression in a pri- guidelines recommend long-term maintenance treat- mary care clinic were found to have greater func- ment to prevent depressive episodes in recurrent tional impairment than those with many other com- is prohibited.
mon medical conditions.[9] Both social adjustment depression.[26-28] Since SAD, by definition, is a re- and quality of life in patients with SAD were signifi- current depressive condition, longer term studies cantly worse than in nondepressed community sam- (i.e. through a full winter season) and maintenance ples, with impairment comparable to patients with or prophylactic treatment studies (to prevent future nonseasonal major depressive disorder.[10,11] The depressive episodes) are very important. In this arti- progressive weight gain experienced by many pa- cle, we review the evidence for longer term and tients with SAD may also lead to greater risk for prophylactic treatment of SAD, focusing on obesity, diabetes and the metabolic syndrome.[12] randomised trials or observational studies with larg- The treatment of SAD is focused on light therapy er sample sizes, and provide clinical strategies for (daily exposure to bright, artificial light)[13] and  2007 Adis Data Information BV. All rights reserved.
Long-Term and Preventative Treatment for SAD used to continue the therapeutic effect of a shortcourse of light therapy.
A major problem with light therapy acute treat- A larger subsequent study also found beneficial ment studies is their short duration of treatment, effects of citalopram in continuation treatment of with placebo-controlled studies ranging from 1 to 5 SAD after bright light therapy.[33] Patients with SAD weeks in duration.[15,16] The short-term antidepres- (n = 269) who were mildly to moderately depressed sant trials and the comparative light versus fluoxe- (scores of 13–22 on the 17-item Hamilton Depres- tine study were also only 8 weeks in length.[17,18,23] sion Rating Scale [HAM-D]) were treated with Few studies have examined treatment for >8 weeks bright light (5000 lux, 2 hours daily) for 7 days.
over the course of the 4–6 month fall/winter season.
Those who responded (n = 168 [62.5%]) with a One exception is a 14-week, open-label study of reduction of ≥50% of the baseline HAM-D score agomelatine, a novel antidepressant with melatonin were then randomised to either citalopram 20–60 MT1 and MT2 receptor agonist and serotonin mg/day (n = 84) or placebo (n = 84) for 15 weeks.
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receptor antagonist properties.[29] Thirty- Relapse rates according to SIGH-SAD criteria were seven outpatients with SAD, as defined by DSM- lower in the citalopram group compared with the IV-TR, and meeting criteria for a moderate to severe placebo group (19.4% vs 31.6%, respectively), but depressive episode, were recruited between the first this did not reach statistical significance. However, week of October and the second week of December.
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relapse rates for other outcome measures (core 6- Patients with a baseline score of ≥22 on the 29-item item subscale HAM-D6: 17.1% vs 31.7%, p < 0.05; version of the Structured Interview Guide for the Melancholia Scale: 16.2% vs 35.1%, p < 0.05) were Hamilton Depression Rating Scale (SAD version; significantly lower in the citalopram-treated group.
SIGH-SAD) were treated with agomelatine 25 mg/ While this suggests that citalopram can be used to original publisher.
day for 14 weeks. The SIGH-SAD scores improved maintain the initial effect of light, the low relapse significantly from week 2 onwards, and after 14 rates in the placebo-treated group indicates that weeks 76% of the patients had responded to treat- some patients with mild symptoms may not show ment (defined as >50% reduction of total SIGH- full relapse after brief treatment with light therapy SAD score) and 70% reached the remission criteria when followed over the course of a winter.
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(SIGH-SAD score <8). These results are promisingbut efficacy of agomelatine will need confirmation in a randomised, placebo-controlled trial.
Most studies of light therapy have shown rapid The regular pattern of depressive episodes in and distribution
relapse (within a week or two) when light is discon- SAD suggests that prevention may be possible, with tinued,[30] leading to clinical recommendations that treatment started in early autumn before the onset of light therapy be continued throughout the winter symptoms, or as soon as the first symptoms of period of risk.[31] However, in some studies, antide- depression appear; however, the depressive episodes pressants have been used to maintain response after of SAD may not be as predictable, as indicated by is prohibited.
initial short-term treatment with light therapy. For retrospectively assessed patterns of episodes. Stud- example, in one pilot study, eight patients with ies show that only 50–70% of patients diagnosed SAD were randomised to citalopram 40 mg/day or with SAD in the summer months or in a previous placebo in combination with ten daily sessions of winter will experience a major depressive episode bright light treatment. After the light treatment on prospective follow-up.[34-37] Depending on the they continued with citalopram or placebo for study design, this means there is a risk of either 1 year.[32] Throughout the follow-up period, the pa- over- or under-estimating the effect of a prevent- tients treated with citalopram had significantly low- ative treatment, since patients may not have a recur- er self-ratings on depressed mood than the patients rence of depression during winter, whether treated receiving placebo, suggesting that citalopram can be or not. Finally, some patients with SAD will also  2007 Adis Data Information BV. All rights reserved.
have occasional nonseasonal episodes, e.g. winter the winter. Of the 11 patients who completed the episodes that extend into the spring and summer, study, eight (73%) reached the relapse criteria on the therefore it is important to determine whether a self-rated Beck Depression Inventory.
preventative treatment needs to continue year- A prevention study using continuous light treat- round, or whether it is only required during the ment involved 38 patients with SAD who had been successfully treated with fluorescent light boxes in Table I summarises the studies on prevention of previous winter seasons.[42] In the early autumn, depressive episodes in SAD. Early studies suggested when not yet depressed, these patients were random- that a brief course of light treatment scheduled at the ly assigned to one of three treatments: (i) light visors first onset of symptoms would be adequate to pre- using bright white incandescent light (2500 lux, 30 vent relapses for the remainder of the winter season.
minutes daily); (ii) identical light visors using infra- In one study, 27 patients experiencing early symp- red light (not known to be an active treatment); and This material is
toms were randomised to 5 days of light therapy (iii) no light treatment. Patients continued with their (2500 lux, 3 hours daily) or to no treatment, and treatment assignment throughout the winter and out- were followed for the rest of the winter.[38] None of come was assessed weekly for 24 weeks using a the 16 light-treated patients developed a depressive self-rated version of the SIGH-SAD, with recur- episode, in contrast to 5 of 11 of the nontreated rence defined as scores ≥20 for 2 consecutive weeks.
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control group. However, this result was not replicat- Of the 30 patients who completed the study, 6 of 14 ed in a study of 17 patients treated with 1 week of (43%) receiving bright light, 5 of 15 (33%) receiv- bright light (10 000 lux, 30 minutes daily) at the first ing infrared light and 6 of 9 (66%) receiving no onset of symptoms and then followed prospective- treatment had recurrence of a depressive episode.
original publisher.
Of the 15 responders to the brief treatment, all Using survival analysis, the infrared treatment was but two relapsed within the 8-week follow-up peri- significantly superior to no treatment (p < 0.02), the bright light had a trend to superiority (p < 0.07)against no treatment and there was no significant Two other small studies examined the prevent- difference between the two light conditions. This ative effect of a brief course of light treatment prior Unauthorised copying
study is limited by the small sample size and the to the onset of symptoms. In one study, 12 patients unexpected result with infrared light, given that it with SAD (previously treated with light therapy was not expected to be an active treatment. Unfortu- during a winter depressive episode) were randomis- nately, no other studies have examined the use of ed in September to either start light treatment when and distribution
they were still well (n = 6) or to start it when theirfirst symptoms of depression occurred (n = 6).[41] In contrast to the very small, methodologically- Bright light (3300 lux, 1 hour daily) was adminis- limited studies of light therapy, there are large, well tered for as long a period as the patient wished.
designed studies of antidepressants for the preven- During the winter follow-up, SIGH-SAD scores tion of depressive episodes in SAD. Preventative is prohibited.
were significantly lower in the group treated with treatment with bupropion XL was examined in three bright light in advance, and none of these patients double-blind, placebo-controlled, multicentre stud- relapsed during the study period.[41] However, a ies in Canada and the US.[43] In total, 1042 patients previous study with a similar design did not find any with SAD diagnosed by clinical history were includ- relapse prevention effect of light treatment adminis- ed in the studies, all of which had identical designs.
tered in September before patients were symptomat- Patients entered the studies between September and ic.[40] Fifteen patients with SAD who had a full November when they were asymptomatic, and were remission to light treatment the previous season seen at least every 4 weeks until the first week of were treated with bright light (2500 lux, 3 hours spring in late March, unless a depressive episode daily) for 5 days and then followed weekly through occurred. Patients were randomised to receive  2007 Adis Data Information BV. All rights reserved.
 2007 Adis Data Information BV. All rights reserved.
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Table I. Studies on the prevention of depressive episodes in seasonal affective disorder
Study design the copyright of the
Long-Term and Preventative Treatment for SAD original publisher.
and distribution
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0/16 (0%) light-treated patients relapsed during follow-up compared with 5/11 (45%) is prohibited.
13/15 (87%) responders to brief treatment Brief treatment given at first onset ofsymptomsPatients followed for 8wk Brief treatment given before onset ofsymptomsPatients followed through one winter Clinical remission was significantly more frequent in the group with bright light given Recurrence rates were significantly lower in Recurrence rates significantly lower in the No significant differences between groups in the recurrence of depressive episodes or RCT = randomised controlled trial.
bupropion XL 150 mg/day or placebo for the first of dry mouth, nausea, constipation and flatulence week, following which those receiving bupropion than placebo. Together, these three studies provide XL were increased to 300 mg/day (if the 300 mg/day good evidence for the efficacy and tolerability of dosage was not tolerated, it could be reduced to 150 bupropion XL as a preventative treatment for de- mg/day). In the first week of spring, the dosage was pressive episodes of SAD when commenced before reduced to 150 mg/day for 2 weeks and then discon- tinued, after which the patients were followed off Of interest is that this is the only SAD study medication by telephone interviews for 8 weeks. A examining discontinuation of treatment in the recurrence of a depressive episode was defined as a spring. In the 8-week follow-up after bupropion was SIGH-SAD ≥20, or fulfilling DSM-IV criteria for stopped, there was no evidence for discontinuation- emergent adverse events. Additionally, depressionrecurrence rates after stopping medications were Results for the three individual studies, as well as very low and no different than placebo (2.7% and a pooled analysis since the study designs were iden- This material is
2.1%, respectively). This indicates that medication tical, are summarised in figure 1. Recurrence rates can be successfully discontinued during the spring were significantly lower for the bupropion XL group than for the placebo group in all three studies (19% Finally, some studies with small sample sizes vs 30% for study A, 13% vs 21% for study B, 16% the copyright of the
have investigated novel treatments for prevention.
vs 31% for study C and 16% vs 28% for the pooled In an RCT (n = 27), the herbal remedy ginkgo biloba sample, respectively). However, survival analyses did not differ from placebo as a preventative treat- for time to onset of depression, comparing bupro- ment for SAD.[44] Another study randomised 23 pion XL with placebo, only reached significance in patients with SAD to 6 weeks of treatment with light study C and in the pooled sample. Furthermore, it original publisher.
therapy, a group-based cognitive behaviour therapy should be noted that the recurrence rates of depres- (CBT) intervention, and the combination of light sive episodes were low overall, even in the placebo- therapy and CBT, and then examined outcomes during the subsequent winter season.[45] All three In these studies, dropout rates for any reason treatments demonstrated significant but similar re- Unauthorised copying
(24% vs 22%) and because of adverse events (9% vs sponses in the short-term treatment trial. However, 5%) did not differ between bupropion and placebo.
at naturalistic follow-up during the subsequent win- Frequencies of adverse events were low overall, ter, patients who had CBT, particularly in combina- with bupropion showing slightly higher frequency tion with light therapy, had better outcomes, as and distribution
measured by symptom severity, remission rates andrelapse rates. This was not a true prevention trialbecause of the naturalistic follow-up in which pa-tients were allowed to use other treatments, but it suggests that CBT may offer some benefits beyond is prohibited.
the short-term treatment phase, in the same way thatCBT may help prevent episodes of nonseasonaldepression.
Seasonal depression is a common and recurrent condition that causes significant morbidity and im- Fig. 1. Bupropion XL vs placebo in the prevention of seasonal
major depressive episodes (MDE) in seasonal affective disorder
pairment of psychosocial function, therefore it is (reproduced from Modell et al.,[43] with permission). reasonable to consider prophylactic and mainte-  2007 Adis Data Information BV. All rights reserved.
Long-Term and Preventative Treatment for SAD nance treatments to prevent depressive episodes.
Better evidence exists for the preventative effica- Complicating the issue, however, is the fact that cy of antidepressants, but only bupropion XL has some patients, even with a history of consecutive been adequately studied and approved for the pre- winter depressive episodes, may not experience a vention of episodes of SAD by regulatory agencies depressive episode in any particular winter. Unfor- (in the US). It is certainly possible that other antide- tunately, there are still limited data to guide clinical pressants (e.g. SSRIs such as fluoxetine and ser- recommendations for the prevention of SAD. There- traline, which show efficacy in short-term treat- fore, the decision to use a preventative treatment ment) are also effective. For antidepressants, pre- must take into account a variety of factors, including ventative treatment should be started in the early individual course and severity of illness, predictabil- autumn at least 4 weeks (the typical time period for ity of episodes and their onset, patient preference response to medications) prior to the usual onset of and motivation, and availability of resources.
symptoms. Extrapolating from the results of thebupropion XL studies, it appears that antidepres- This material is
Similarly, the choice of preventative treatment sants can be safely tapered and discontinued in the requires individual assessment to weigh potential spring (at the time of usual remission) and summer.
benefits against risks of adverse effects. For exam- Discontinuation symptoms, however, may vary ple, light therapy may be the treatment of choice for among different antidepressants and it is important patients who prefer nonpharmacological treatment, the copyright of the
to distinguish these from depressive symptoms, in- have relative contraindications to drug therapy (e.g.
dicating recurrence. It may be more prudent to con- hepatic disease) or are intolerant to medication ad- tinue the antidepressant year-round for individual verse effects. On the other hand, medication treat- patients if they have usual remission of symptoms ment may be the treatment of choice for patients later in the spring, require longer taper periods (e.g.
who cannot make the time commitment for light original publisher.
those on higher doses or those who experience sig- therapy, have relative contraindications to light ther- nificant discontinuation symptoms), or have subsyn- apy (e.g. retinal disease, macular degeneration, use dromal symptoms in the summer, as the time off of photosensitising medications) or are intolerant to medication will be very short. In this situation, pa- the adverse effects of bright light.
tients should be cautioned about the possibility of Unauthorised copying
There are only limited efficacy data for longer term and preventative treatment with light therapy.
In clinical practice it is also common to combine Because light therapy has a fast onset of action light and antidepressant treatment.[46] Unfortunately, (from a few days to 1 or 2 weeks), it is reasonable to no studies have examined the effect of combination and distribution
recommend starting light therapy at the time of first use of light therapy and antidepressants, either for onset of symptoms in the autumn; however, some short-term or maintenance treatment. In addition, patients have rapid onset of symptoms or may not there is a suggestion that CBT may also offer bene- recognise the insidious onset of depression until fits for the prevention of SAD. These will be impor- they are in a full episode. These patients may want tant future research directions for the field.
is prohibited.
to restart their light therapy at least 2 weeks (thetypical time period for response to light) ahead of their usual onset of depressive symptoms. There isno good evidence that a brief course of light therapy Longer term and preventative treatments for pa- can prevent relapse, therefore light treatment should tients with SAD are indicated because of the dura- be continued throughout the winter season and dis- tion and recurrent pattern of winter depressive epi- continued during spring and summer. Alternatively, sodes. Unfortunately, there is less evidence for effi- a brief course of light treatment can be followed by cacy of light therapy and antidepressants in continuation treatment with antidepressant medica- continuation and maintenance phases than for acute treatment of SAD. Hence, clinical recommendations  2007 Adis Data Information BV. All rights reserved.
6. Levitt AJ, Boyle MH. The impact of latitude on the prevalence are based on a limited number of quality studies and of seasonal depression. Can J Psychiatry 2002; 47 (4): 361-7 by extrapolating from acute studies. A complicating 7. Sohn CH, Lam RW. Update on the biology of seasonal affective factor is the variable predictability of self-reported disorder. CNS Spectr 2005; 10 (8): 635-46 8. Lam RW, Levitan RD. Pathophysiology of seasonal affective seasonal patterns of illness, since prospective moni- disorder: a review. J Psychiatry Neurosci 2000; 25 (5): 469-80 toring indicates that only about 30–70% of patients 9. Schlager D, Froom J, Jaffe A. Winter depression and functional impairment among ambulatory primary care patients. Compr with SAD will have recurrence of a winter depres- sive episode. Therefore, the need for, and choice of 10. Pendse BP, Ojehagen A, Engstrom G, et al. Social characteris- preventative treatment relies on clinical judgement tics of seasonal affective disorder patients: comparison withsuicide attempters with non-seasonal major depression and consideration of various factors, including indi- and other mood disorder patients. Eur Psychiatry 2003; 18 (1): vidual course and severity of illness, predictability of episodes and their onset, patient preferences and 11. Michalak EE, Wilkinson C, Hood K, et al. Seasonality, negative life events and social support in a community sample. Br J motivation, and availability of resources.
Given the significant personal and psychosocial 12. McElroy SL, Kotwal R, Malhotra S, et al. Are mood disorders This material is
and obesity related? A review for the mental health profession- impairment associated with SAD, it is important to al. J Clin Psychiatry 2004; 65 (5): 634-51 conduct further studies to determine which patients 13. Terman M, Terman JS. Light therapy for seasonal and non- need maintenance treatment and how to optimise seasonal depression: efficacy, protocol, safety, and side ef-fects. CNS Spectr 2005; 10 (8): 647-63 preventative treatment with light therapy and/or 14. Pjrek E, Winkler D, Kasper S. Pharmacotherapy of seasonal the copyright of the
affective disorder. CNS Spectr 2005; 10 (8): 664-9 15. Thompson C. Evidence-based treatment. In: Partonen T, Mag- nusson A, editors. Seasonal affective disorder: practice and research. New York; Oxford University Press, 2001: 151-8 16. Golden RN, Gaynes BN, Ekstrom RD, et al. The efficacy of Dr Westrin is funded by a fellowship award from Lund light therapy in the treatment of mood disorders: a review and University Medical Faculty, Region Sk˚ane and Ellen och original publisher.
meta-analysis of the evidence. Am J Psychiatry 2005; 162 (4): Henrik Sj¨obrings Minnesfond, and has no conflicts of interest that are directly relevant to the content of this review. Dr Lam 17. Lam RW, Gorman CP, Michalon M, et al. Multicenter, placebo- is on speaker/advisory boards for, or has received research controlled study of fluoxetine in seasonal affective disorder.
funds from, ANS, Inc., AstraZeneca, Biovail, Canadian Insti- 18. Moscovitch A, Blashko CA, Eagles JM, et al. A placebo- tutes of Health Research, Canadian Network for Mood and Unauthorised copying
controlled study of sertraline in the treatment of outpatients Anxiety Treatments, Eli Lilly, GlaxoSmithKline, GreatWest with seasonal affective disorder. Psychopharmacology (Berl) Life, Janssen, Litebook Company, Inc., Lundbeck, Sanofi- Aventis, Servier, VGH and UBC Hospital Foundation, and 19. Hilger E, Willeit M, Praschak-Rieder N, et al. Reboxetine in Wyeth. He has stock options in Litebook Company, Inc. No seasonal affective disorder: an open trial. Eur Neuropsy- sources of funding were used to assist in the preparation of 20. Lingjaerde O, Reichborn-Kjennerud T, Haggag A, et al. Treat- and distribution
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Rosenthal NE, Sack DA, Gillin JC, et al. Seasonal affective 22. Partonen T, Lonnqvist J. Moclobemide and fluoxetine in treat- disorder: a description of the syndrome and preliminary find- ment of seasonal affective disorder. J Affect Disord 1996; 41 ings with light therapy. Arch Gen Psychiatry 1984; 41 (1): 72- 23. Lam RW, Levitt AJ, Levitan RD, et al. The Can-SAD Study: a 3. Magnusson A, Partonen T. The diagnosis, symptomatology, and randomized controlled trial of the effectiveness of light therapy epidemiology of seasonal affective disorder. CNS Spectr 2005; and fluoxetine in patients with winter seasonal affective disor- der. Am J Psychiatry 2006; 163 (5): 805-12 4. Blazer DG, Kessler RC, Swartz MS. Epidemiology of recurrent 24. Frank E, Prien RF, Jarrett RB, et al. Conceptualization and major and minor depression with a seasonal pattern. The rationale for consensus definitions of terms in major depres- National Comorbidity Survey. Br J Psychiatry 1998; 172: 164- sive disorder: remission, recovery, relapse, and recurrence.
5. Levitt AJ, Boyle MH, Joffe RT, et al. Estimated prevalence of 25. Parikh SV, Lam RW. Clinical guidelines for the treatment of the seasonal subtype of major depression in a Canadian com- depressive disorders: I. Definitions, prevalence, and health munity sample. Can J Psychiatry 2000; 45 (7): 650-4 burden. Can J Psychiatry 2001; 46 Suppl. 1: 13-20S  2007 Adis Data Information BV. All rights reserved.
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