E-Pie: Pathology Information Exchange
News in Brief
Clinical Case Discussion
Diagnostic Tests
Oral Pathology Seminars
Miscellaneous
Home

 

Case of the Month
Past Issues
OMS Pathology Services Home

 

Miscellaneous

Do You Have SAD Patients in Your Office?

M. Michele Murburg, MD

The dark days of winter are likely depressing a significant number of your patients, and maybe others in your life. Seasonal Affective Disorder (SAD) affects approximately 4% to 6% of the general population, with subsyndromal features manifested by an additional 10% to 20% (1). Among patients with a history of recurrent mood disorders, the prevalence may be as high as 38% (2-4). SAD is considerably more prevalent in latitudes farther from the equator (e.g.: 9.7% in New Hampshire, compared with 1.4% in Florida) (5), and disproportionately afflicts younger people and women (6). The diagnosis of SAD is made (or, to be technical, the DSM-IV "Seasonal Pattern Specifier" is appended to the diagnoses of bipolar or major depressive disorder) when, during the last 2 years or longer, patients show a seasonal pattern of major depressive episodes that usually begin in fall or winter and remit in spring without any nonseasonal episodes in the interim, and when the episodes are not explained by seasonally linked psychosocial stressors (6). In "winter depression" symptoms include anergy, hypersomnia, overeating, weight gain, and a craving for carbohydrates (6).

Although the pathogenesis of SAD has not been well elucidated, an increasing amount is becoming known about biological abnormalities associated with the disorder. Some evidence suggests that SAD may involve mechanisms that mediate seasonal variations in the biology and behavior (such as, perhaps, hibernation) of other mammalian species. Wehr et al (7) have shown that patients with SAD, excepting normal volunteers, generate a biological signal of change of season (an increase in nocturnal melatonin secretion in winter compared with summer) similar to the signal that mammals use to regulate seasonal changes in their behavior, and conclude that "neural circuits that mediate the effects of seasonal changes in day length on mammalian behavior [may] mediate effects of season and light treatment on seasonal affective disorder." Some attempts to treat SAD with agents, such as beta adrenergic blockers that lower Melatonin secretion, have shown a degree of promise (8), but more research is needed, particularly since some beta blockers have Serotonin enhancing effects as well. There is in fact a great deal of evidence that the neurotransmitter Serotonin is involved in the pathogenesis of SAD (9). Hypothalamic Serotonin levels have been found to decrease in the fall and throughout the winter (10). Depressive symptoms can be provoked in SAD patients (and in patients with other forms of Major Depression) by induced depletion of L-tryptophan, the amino acid precursor of Serotonin (11), while serotonergic agents, including selective Serotonin reuptake inhibitors (SSRI's), improve SAD symptoms (12-15). Willeit et al (16) recently reported that a polymorphism (5-HTTLPR) in the serotonin transporter promoter gene is associated with DSM-IV depression subtypes in seasonal affective disorder, and concluded that their data were "compatible with the hypothesis of a disease process that is not causally related to 5-HTTLPR, but involves 5-HT neurotransmission and 5-HTTLPR somewhere on its way to phenotypic disease expression."

Whatever neurochemical and genetic mechanisms may be involved, however, SAD symptoms appear to be induced by lessened amounts of daylight, and can be remitted with adequate light exposure or "treatment" (17). 10,000 lux white fluorescent light for 30 minutes in the early morning, usually between 7 and 8 am, is as safe and effective as Fluoxetine for the treatment of seasonal affective disorder (SAD), according to a recent randomized trial by Lam and associates (18). However, given the inconvenience of early morning light therapy for many patients, other effective light strategies have been tested. Avery (19) reported that “bright light (2500 lux) given in the workplace improves subjective ratings of mood, energy, alertness and productivity in SAD subjects. Morning and afternoon bright lights resulted in similar levels of improvement.” Light therapy has the advantage of lacking drug side effects, but antidepressants, particularly the SSRIs, are also effective (20). While light boxes and SSRIs may seem simple interventions, psychiatric referral of patients with SAD is also a good idea, particularly as mania can emerge in the course of treatment with either modality and is not always accurately predicted by known past history.

References

  1. Kasper S, Wehr TA, Bartko JJ, et al. Epidemiological findings of seasonal changes in mood and behavior. Arch Gen Psychiatry. 1989; 46:823-33.
  2. Faedda GL, Tondo L, Teicher MH, et al. Seasonal mood disorders: patterns of seasonal recurrence in mania and depression. Arch Gen Psychiatry. 1993; 50:17-23.
  3. Kasper S, Kamo T. Seasonality in major depressed inpatients. J Affect Disord. 1990; 19: 243-8.
  4. Garvey MJ, Wesner R, Godes M. Comparison of seasonal and nonseasonal affective disorders. Am J Psychiatry. 1988; 145: 100-2.
  5. Rosen LM, Targum SD, Terman M, et al. Prevalence of seasonal affective disorder at four latitudes. Psychiatry Res. 1989;31: 131-44.
  6. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, American Psychiatric Association, Washington DC, 1994, pp389-390.
  7. Wehr TA; Duncan WC; Sher L; Aeschbach D; Schwartz PJ; Turner EH; Postolache TT; Rosenthal NE : Arch Gen Psychiatry 2001 Dec;58(12):1108-14
  8. Schlager DS. Early-morning administration of short-acting ß-blockers for the treatment of winter depression. Am J Psychiatry. 1994; 151:1383-5.
  9. O'Rourke DA, Wurtman JJ, Brzezinski A, et al. Serotonin implicated in etiology of seasonal affective disorder. Psychopharmacol Bull. 1987; 23:358-9.
  10. Carlsson A, Svennerholm L, Winblad B. Seasonal and circadian monoamine variations in human brains examined post-mortem. Acta Psychiatr Scand. 1980; 61:75-85.
  11. Neumeister A, Praschak-Rieder N, Hesselmann B, et al. Effects of tryptophan depletion in fully remitted patients with seasonal affective disorder during summer. Psychol Med. 1998; 28:257-64.
  12. Lam RW, Gorman CP, Michalon M, et al. Multicenter, placebo-controlled study of fluoxetine in seasonal affective disorder. Am J Psychiatry. 1995;
    152: 1765-70.
  13. McGrath RE, Buckwald B, Resnick EV. The effect of L-tryptophan on seasonal affective disorder. J Clin Psychiatry. 1990; 51:162-3.
  14. Moscovitch A, Wiseman RL, Glodberg MS, et al. A double-blind, placebo-controlled study of sertraline in the treatment of outpatients with SAD [abstract]. Presented at: American Psychiatric Association Meeting; Miami Beach, Fla; May 24, 1995.
  15. Wirz-Justice A, VanderVerle P, Bucher A, et al. Comparison of light treatment with citalopram in winter depression: a longitudinal single case study. Int Clin Psychopharmacol. 1992;7: 109-16.
  16. Willeit M; Praschak-Rieder N; Neumeister A; Zill P; Leisch F; Stastny J; Hilger E; Thierry N; Konstantinidis A; Winkler D; Fuchs K; Sieghart W; Aschauer H; Ackenheil M; Bondy B; Kasper S: A polymorphism (5-HTTLPR) in the serotonin transporter promoter gene is associated with DSM-IV depression subtypes in seasonal affective disorder. Mol Psychiatry 2003 Nov;8(11): 942-6.
  17. Tam EM, Lam RW, Levitt AJ. Treatment of seasonal affective disorder: a review. Can J Psychiatry. 1995: 40:457-66.
  18. Lam RW: Light Therapy as Effective as Fluoxetine for Seasonal Affective Disorder CPA 54th Annual Meeting: Paper PS7D. Presented Oct. 16, 2004
  19. Avery DH; Kizer D; Bolte MA; Hellekson C: Bright light therapy of subsyndromal seasonal affective disorder in the workplace: morning vs. afternoon exposure. Acta Psychiatr Scand 2001 Apr; 103(4):267.
  20. Jepson TL, Ernst ME, Kelly MW: Current Perspectives on the Management of Seasonal Affective Disorder. J Am Pharm Assoc 1999:39(6): 822-829.