A 30-year-old woman with severe pathological gambling and cyclothymia presented to our program with no previous history of pharmacologic or psychotherapeutic treatment. Pathological gambling is an impulse-control disorder not otherwise specified (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) in which comorbidity is common, particularly with substance abuse, obsessive-compulsive disorder and mood disorders. As described in this case, pathological gamblers with bipolar comorbidity may be effectively treated with mood stabilizers such as lithium. After receiving 10 weeks of lithium treatment, the patient showed improvement in both gambling behavior and affective instability. The identification of specific subtypes among patients with pathological gambling may be relevant to the choice of pharmacologic treatment.

Since 1984, 447 articles have been published using the acronym “SAD” for seasonal affective disorder in the heading of the publication, and since 1992, 59 articles have used “SAD” in the heading of the publication as an acronym for social anxiety disorder, according to MEDLINE. Using the acronym SAD for social anxiety disorder has been used with more frequency in recent scientific publications—interestingly, mostly in connection with newer antidepressants that have been found to be of therapeutic potential for this indication. To avoid possible confusions in research, the acronym “SOAD” was proposed for social anxiety disorder by Kasper and Winkler and “SAnD” by Nutt (D.J. Nutt, MD, PhD, unpublished data, 2004)—seemingly without success since these abbreviations are not seen in the literature. This month, CNS Spectrums focuses on the existing literature on the original acronym for SAD—seasonal affective disorder and its worldwide recognition.

In the early 1980s, Rosenthal and colleagues at the National Institute of Mental Health (NIMH) set out to describe a syndrome called SAD, not to be confused with the other, more recent SAD, social anxiety disorder. The original has been known to physicians since ancient times, dating back to Aretaeus the Cappadocian. However, the NIMH researchers for the first time systematically described the clinical symptomatology, compared it with healthy controls, and differentiated SAD from nonseasonal depression. Their work in tandem with emerging technology led to the discovery of the underlying pathophysiology of SAD and treatment approaches. The most important of these approaches were light therapy and pharmacotherapeutic options.

The operational criteria for seasonal affective disorder (SAD) have undergone several changes since first proposed in 1984. SAD is currently included as a specifier of either bipolar or recurrent major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The International Classification of Diseases, Tenth Edition has provisional diagnostic criteria for SAD. The most characteristic quality of SAD is that the symptoms usually present during winter and remit in the spring. Furthermore, the symptoms tend to remit when the patients are exposed to daylight or bright light therapy. The cognitive and emotional symptoms are as in other types of depression but the vegetative symptoms are the reverse of classic depressive vegetative symptoms, namely increased sleep and increased appetite. SAD is a common condition, but the exact prevalence rates vary between different studies and countries and is consistently found to be more common in women and in youth. SAD probably possibly occurs in children although not as commonly as in young adults. Some studies have found that certain ethnic groups who live at high northern latitudes may have adapted to the long arctic winter.

The etiology and pathophysiology of seasonal affective disorder (SAD) has been linked to the seasons and to light since its first conceptualization. Aspects of SAD that make it particularly amenable to biological investigation include the predictable recurrent episodes, the rapid response to a nonpharmacologic treatment, the specific neurovegetative features, and the availability of rich animal models of seasonality. This paper reviews new findings for the major biological hypotheses for SAD, focusing on circadian rhythms, neurotransmitters, and molecular genetics. Integrative issues and future directions for the study of SAD, including the heuristic value of a dualvulnerability hypothesis that conceptualizes seasonality as a dimensional construct and the importance of studying endophenotypes, will be discussed.

Bright light therapy for seasonal affective disorder (SAD) has been investigated and applied for over 20 years. Physicians and clinicians are increasingly confident that bright light therapy is a potent, specifically active, nonpharmaceutical treatment modality. Indeed, the domain of light treatment is moving beyond SAD, to nonseasonal depression (unipolar and bipolar), seasonal flare-ups of bulimia nervosa, circadian sleep phase disorders, and more. Light therapy is simple to deliver to outpatients and inpatients alike, although the optimum dosing of light and treatment time of day requires individual adjustment. The side-effect profile is favorable in comparison with medications, although the clinician must remain vigilant about emergent hypomania and autonomic hyperactivation, especially during the first few days of treatment. Importantly, light therapy provides a compatible adjunct to antidepressant medication, which can result in accelerated improvement and fewer residual symptoms.

Seasonal affective disorder is a common variant of recurrent major depressive disorder or bipolar disorder. Treatment with bright artificial light has been found to be effective in this condition. However, for patients who do not respond to light therapy or those who lack compliance, conventional drug treatment with antidepressants also has been proposed. Substances with selective serotonergic or noradrenergic mechanisms should be preferred over older antidepressants. Although there are a number of open and controlled studies evaluating different compounds, these studies were often limited by relatively small sample sizes. Furthermore, there are no studies specifically addressing bipolar seasonal depression. This article will review the published literature on pharmacotherapy of seasonal affective disorder.