SAD Autumn Onset, Winter Gloom - Board Review

A subtype of major depressive disorder, seasonal affective disorder (SAD) may affect 6% of the North American population. In most cases, onset occurs in autumn or early winter, and the condition remits in spring. Delayed circadian rhythms, abnormal regulation of certain neurotransmitters, and genetics all appear to contribute to the pathogenesis of SAD; seasonal depletion of daylight is a key contributing factor. Criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) are generally used to diagnose patients with SAD. Bright-light therapy is considered first-line treatment, possibly combined with antidepressive agents.

In the United States, 5% to 12% of men and 10% to 25% of women experience a major depressive episode in their lifetime; direct and indirect costs of depression have been estimated at $43.7 billion per year. (1) According to data from the National Comorbidity Survey, only 27.7% of patients with major depression, ages 14 to 55 years, receive outpatient mental health services. (2) Not surprisingly, depressive disorders are frequently encountered in the primary care setting. One major depressive disorder subtype that is characterized by re-current seasonal patterns is seasonal affective disorder (SAD).

SAD is classified into two discernible types. The more common form, called fall-onset or winter depression, classically begins in late autumn and abates in the spring and summer. In most cases, its symptoms are dosely related to those of atypical depression. (3) Patients experience increased sleep, increased appetite, craving for carbohydrates, weight gain, and interpersonal conflict. Other symptoms include irritability and heaviness in the extremities (referred to as leaden paralysis.) (3,4)

The second type, which is far less common, is called spring-onset SAD. The depressive episode generally begins in late spring or early summer and lasts through early fall. Patients'' symptoms are characteristic of a typical depressive disorder and include insomnia, weight loss, and poor appetite. (5)

Clinicians must be attentive to the possible signs and symptoms of SAD, to ensure early diagnosis and appropriate therapy.

Epidemiology

Estimated incidence of SAD in the general population in North America is about 6%, ranging latitudinally (south to north) from 2% to 10% (6-8); an additional 10% to 20% may experience subsyndromal features of SAD. The occurrence of seasonal changes in mood and behavior appears to increase in the northern latitudes. One early study, for example, showed a 1.4% incidence of SAD among Florida residents, compared with 9.7% among residents of New Hampshire. (9) By some estimates, however, the incidence of SAD in North America is double that in Europe--suggesting that climate, culture, and genetics may be more important factors. (10)

Incidence of SAD is reportedly highest among patients with a history of recurrent mood disorders. (6) SAD affects about four women for every man with the disorder; however, men with SAD are more likely to experience major depressive episodes. (4) Compared with younger adults, elderly people appear to have relatively minor seasonal fluctuations in psychological well-being. (6,11)

In children and adolescents, SAD has not been studied adequately and is not well understood. Children with SAD are reported to have enormous cravings for carbohydrates, to experience severe mood swings, and to be extremely irritable. The condition may be under-recognized in younger patients because some signs--tantrums, hyperactivity, and over-tiredness--mimic common childhood behaviors or signs of other disturbances. Labile hormonal changes that occur during puberty may mask symptoms of SAD in adolescents. (12) Clinicians need to keep a high level of suspicion for SAD during late autumn when behavioral issues arise among children and adolescents in their care.

In adult patients, possible indicators of SAD include fatigue, depressed affect, and loss of interest in routine activities, especially during the fall. Although it is not dear whether SAD is an inherited disorder, results from one study of adult twins suggest that genetics may account for at least 29% of "seasonality" in men and women. (13)

The Etiological Conundrum

Conflicting results in ongoing studies of various explanations for SAD have led researchers to call it a "biologically heterogeneous condition"--the possible result of both seasonality and depression. (14) Most theories associate shorter daylight periods and winter''s diminished amounts of sunlight with depressive episodes (3,6); the response of most SAD patients to artificial bright-light therapy supports this line of thought. (15) Hypotheses to explain SAD include shifting patterns in daily biochemicals, excessive or inadequate regulation of certain neurotransmitters, and genetic influence. (14)

The human brain, research shows, has a precise, 24-hour repeating rhythm to regulate daytime and nighttime activities. The biochemical circadian rhythm relies on brain function to manage core body temperature, release hormones, and trigger other processes. At night, circadian rhythm mechanisms lower body temperature and trigger production of melatonin, a hormone secreted by the pineal gland that enhances sleep. (16)

It has been hypothesized that these circadian rhythms in SAD patients are delayed during the winter months when sunlight is diminished. Exposure to bright light in the morning hours often seems to correct these rhythms--although the exact mechanism of action is not clearly understood. (6,14) Numerous environmental factors may affect circadian rhythms, including sleep, physical activity, and eating. (14)

It was once hypothesized that irregularities in melatonin secretion might explain SAD--that is, until it was shown that winter melatonin rhythms do not differ between SAD patients and other persons. (17) Recent evidence suggests that impaired or altered transmission of the neurotransmitters serotonin, dopamine, norepinephrine, and/or neuropeptide Y ma cause a disruption of biological rhythms. (14) Low levels of serotonin, for example, can induce depression--and levels decline in late autumn and throughout the winter months. The association between carbohydrate ingestion and increased serotonin levels may explain SAD patients'' craving for carbohydrates. (18)

Preliminary findings associating specific genes with seasonality and related behaviors are promising, but they must be reproduced in larger controlled studies. (13,14)

Diagnostic Criteria for SAD

The components of SAD are described in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). (19) SAD is a subtype of major depressive disorder. The patient must have experienced a regular seasonal-related pattern of depression during the previous two years, with episodes generally beginning in the fall or winter and remitting in spring. Patients may have had a previous diagnosis of depressive disorder or may give a detailed history of depressive symptoms with fall onset for at least two years. (4) The DSM-IV criteria for a major depressive episode and for seasonal pattern specifier are listed in Tables 1 and 2 (19) (see pages 52 and 53).

Although in the clinical setting the DSM-IV criteria are now most commonly used to diagnose SAD, other assessment tools are available, eg, the Personal Inventory for Depression and SAD (20,21) (PIDS, available at www.cet.org/pids.htm). The Structured Interview Guide for the Hamilton Depression Rating Scale--Seasonal Affective Disorder Version (SIGH-SAD) is expanded from the Hamilton scale to measure symptom severity. (22) In Canada, where every university hospital has a SAD clinic, (23) national SAD management guidelines cite the Seasonal Pattern Assessment Questionnaire (24) (SPAQ) as simple and useful but recommend careful clinical evaluation to confirm the diagnosis of SAD. (6)

Treatment of SAD

First-line treatment for the patient with confirmed SAD is bright-light therapy. (6,23,25) This modality is defined as exposure to visible light of at least 2,500 lux (units of illumination) at eye level. Apparently it is the eyes, not the skin, that mediate the effects of bright-light therapy. (26) As light passing through the pupil is absorbed by the retina, increased neuromotor activity lessens symptoms of SAD. (14)

Light boxes manufactured for SAD therapy produce 2,500 to 10,000 lux. (23) Acceptable light boxes must filter out potentially harmful ultraviolet rays. Light visors produce lower levels of light than standard light boxes--but they are used closer to the eyes. This apparatus has not yet been shown to be efficacious in reducing symptoms of SAD. (27)