Evidence-Based Reviews

SAD: Is seasonal affective disorder a bipolar variant?

Current Psychiatry. 2010 February;9(2):43-54

References

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Cassidy and Carroll¹⁰ measured the frequency of mood episodes in 304 BD patients not assessed for seasonality. Manic episodes peaked in early spring, mixed episodes peaked in late summer or fall, and depressive episodes peaked in fall-winter.

Irregular rhythm. Both BD and MDD SP involve irregularities in daily or circadian rhythms, such as changes in the timing of sleep, melatonin release, and body temperature.^3,5,11 Circadian phase delays—in which internal rhythms lag behind the sleep cycle—are correlated with symptom severity in BD¹² and are implicated in the core pathology of BD¹³ ( Box 2 ). In BD, life events that change social rhythms may disrupt circadian rhythms, triggering mood episodes.⁵

Etiologic hypotheses for both BD and SAD propose that an external event (life stress in BD; decreased photoperiod in SAD) leads to circadian dysregulation and, in turn, mood episodes. Circadian-related hypotheses for SAD and BD are supported by evidence showing efficacy of treatments that manipulate behavioral and circadian rhythms.

Box 1

Seasonal affective disorder: A depression continuum
from unipolar to bipolar?

Seasonality refers to the degree of seasonal changes in behavior and mood within an individual. Seasonality scores are normally distributed,^a suggesting that seasonality may be continuous in the general population—with some individuals meeting criteria for a seasonal mood disorder:

A seasonal pattern is reported by approximately 10% to 20% of depressed outpatients with recurrent mood disorders and an estimated 15% to 22% of individuals with bipolar disorder (BD).^b
Persons with BD—seasonal or not—report greater seasonality compared with those with major depressive disorder (MDD).^c

Among individuals with seasonal affective disorder, the course is bipolar in an estimated 12% to 22% and unipolar in 78% to 88%.^d These estimates may reflect underdiagnosis of BD with seasonal pattern because hypomania is difficult to diagnose retrospectively.^e

The bipolar-unipolar continuum includes (in order): BD I, BD II, bipolar disorder not otherwise specified, cyclothymia, bipolar spectrum disorder, and MDD.^f In examining the validity of the bipolar spectrum model, Phelps et al^g noted:

At least 3 studies found that all symptoms reported by individuals with unipolar and bipolar diagnoses approach a normal distribution, rather than a bimodal distribution separating unipolar from bipolar symptom profiles.
Data from 2 population-based studies indicate that subthreshold hypomanic symptoms are more common than and cause as much impairment as symptoms meeting criteria for BD II or I.

Some individuals who meet criteria for MDD with seasonal pattern have summertime periods of transient hypomania and hyperthymia (hypomanic-like periods without clinically significant impairment).^h This suggests that the bipolar continuum also may exist among individuals with seasonal pattern mood disorders.

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Box 2

Proposed mechanisms for seasonal affective disorder

Etiologic hypotheses of seasonal affective disorder (SAD) include:

photoperiodic hypothesis (shorter winter days cause SAD,^a perhaps mediated by a summer vs winter difference in duration of nightly melatonin release)^b
phase shift hypothesis (less available light in winter may lead to an inability to synchronize circadian rhythms with sleep/wake rhythms).^c

Some case studies of rapid-cycling bipolar disorder (BD) suggest that mood is correlated with daily hours of sunshine and light therapy is antidepressant. Rapid-cycling patients may be hypersensitive to day-to-day changes in photoperiod, analogous to mood changes in response to changes in photoperiod across the seasons in SAD.^d

Circadian phase delays—in which internal rhythms lag behind the sleep cycle—are correlated with symptom severity in BD^e and are implicated in the core pathology of BD.^f Phase delays also are present in some individuals with SAD and are associated with severity and treatment response.^g Preliminary evidence suggests that variation in circadian clock genes is related to both BD^f,h and SAD.ⁱ

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CASE CONTINUED: Seasonal pattern revealed

Ms. S was aware that she is vulnerable to depressive episodes in fall and winter but unaware of a pattern of hypomanic/manic episodes in spring and summer. Her family psychiatric history includes a sister diagnosed with BD I (with no seasonal specifier), and a maternal aunt who has attempted suicide several times.

Ms. S agrees to an assessment plan including a diagnostic interview, interviews measuring symptom severity and pattern of recurrence, routine laboratory examination, and self-report questionnaires. These show that she meets DSM-IV-TR criteria for BD I, depressed, moderate, with seasonal pattern.

Clinical Point

In patients with SAD, screen for bipolarity (such as with the HIGH-SAD tool) to avoid triggering mania or hypomania during treatment

Her assessment scores are 28 on the Structured Interview Guide for HDRS-seasonal affective disorder version (SIGH-SAD), 17 on the Hamilton Depression Rating Scale (HDRS), and 11 on the atypical subscale. The HDRS and atypical subscale are components of the SIGH-SAD reflecting typical (eg, insomnia, loss of appetite, etc.) and atypical (eg, hypersomnia, increased appetite, etc.) depression symptoms, respectively. Ms. S’s scores exceed the threshold scores defining a BD SP episode (>20 SIGH-SAD + >10 HDRS + >5 atypical subscale¹⁴). Data from self-report questionnaires corroborate this assessment.