Seasonal Affective Disorder
Introduction
Depression, fatigue and lassitude during the long dark nights and short dim days of winter has been recognized in the northern latitudes since ancient times. It was described in the Goths of the 6th century by the Roman historian Jordanis, and has been a well-known clinical phenomenon in Scandinavia, but did not attract systematic attention until 1970, when engineer Herb Kern deduced through detailed recording of mood symptoms that his recurrent episodes of depression and hypomania followed a cyclical pattern of corresponding to the seasons. National Institute of Mental Health psychiatrist Norman Rosenthal, who had himself experienced seasonal depression after moving from South Africa to New York, hypothesized that the mood cycling might be driven by day length, and they were able to ameliorate wintertime depression with increased day length through exposure to fluorescent lights (Marshall & Cheevers, 2003). Recruitment for a placebo-controlled trial identified a large group with similar symptoms, and suggested that seasonal cycling of mood was not uncommon (Rosenthal, Sack, Gillin, Lewy, Goodwin, Davenport, Mueller, Newsome & Wehr, 1984). Subsequent studies have shown a an inverse correlation with daylight length in almost all countries, a relationship with degree of cloud cover and evidence of circadian rhythm disturbances that can be rectified with light exposure (Lam & Levitan, 2000). Seasonal depression in summer and fall that remits in winter and spring has also been described, as well as the less frequent occurrence of seasonal mood cycling in children (Magnusson & Partonen, 2005). Diagnostic criteria for seasonal affective disorder were developed for the third revision of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1987), and in the most recent fifth revision (American Psychiatric Association, 2013) the condition is a “course specifier” which further defines a diagnosis of Bipolar Disorder or Major Depressive Disorder by the presence of “seasonal features”.
Symptoms
People with seasonal affective disorder have normal mental health for most of the year but experience recurrent depressive symptoms in the winter. Smaller numbers of patients have summer and fall exacerbations. Hypersomnia, overeating and lack of energy are most common, along with depressed mood, anxiety, irritability, anhedonia, withdrawal from usual activities and interests and decreased sex drive. Most patients with seasonal affective disorder meet DSM-5 criteria for major depressive disorder, but 20 per cent are found to meet criteria for bipolar 1 or 2 disorder. About 25 per cent of bipolar patients have seasonal depressive episodes, which are associated with bipolar 2 disorder, frequent depressive episodes, rapid cycling of moods or eating disorders, Male patients with seasonal features tend to have bipolar 2 disorder and more frequent depressive episodes, while rapid cycling and eating disorders are more common in female seasonal patients (Geoffroy, Bellevier, Scott, Boudebesse, Lajnef, Gard, Kahn, Azorin, Henry, Laboyer & Etain, 2013).
Summer and winter affective disorders have slightly different symptoms. The winter-onset disorder includes depression, hopelessness, anxiety, difficulty concentrating, social withdrawal and lack of interest in customary activities, lack of energy, limb heaviness and appetite change (usually increased) with carbohydrate craving and weight gain. Seasonal depression with spring or summer onset commonly features anxiety, insomnia, agitation, irritability, decreased appetite and weight loss and increased sex drive. Bipolar patients with seasonal exacerbations in spring or summer may have mania or hypomania more often than those with winter cycling, who are more prone to depressive symptoms (Faedda, Tondo, Teicher, Baldessarini, Gelbard & Floris, 1993). Seasonal depression, and less frequently hypomania, is occasionally seen in children, usually manifested by school problems, insomnia and less often hypersomnia, irritability and fatigue, often ascribed by the patients to family and school situations (Swedo, Allen, Glod, Clark, Teicher, Richter, Hoffman, Hamburger, Dow, Brown & Rosenthal, 1997). Many patients have hyperthymia in between depressive episodes, which may not be sufficient to identify as hypomania and, since it is often adaptive and even agreeable to the patient, may not come to medical attention (Partonen & Rosenthal, 2001).
Diagnostic Criteria
Seasonal Affective Disorder was incorporated into DSM-III as a “seasonal pattern” modifier of other diagnoses of recurrent mood disorder, in order to recognize that patients might have bipolar disorder or major depression but also seasonal variability of mood (American Psychiatric Association, 1987). An argument has been made that patients with seasonal mood disorders have differences in ocular light processing, seasonal changes in melatonin secretion and deficient serotonin neurotransmission that can be reversed with light exposure, such that seasonal affective disorder ought to be an independent condition (Rosenthal, 2009). It has been decided in the preparation of the DSM-5 that seasonal affective disorder should remain a “course modifier” of bipolar disorder or major depression, due to the accumulation of evidence that the mood symptoms of seasonally- afflicted patients are very much like those of others with mania, hypomania or depression, only more clearly linked to the season and to ambient light (Roecklein & Rohan, 2005).
Patients who meet the DSM-5 criteria for recurrent major depressive disorder, bipolar 1 disorder or bipolar 2 disorder (American Psychiatric Association, 2013) can be assessed by different criteria for a “seasonal subspecifier”. This means that a regular temporal relationship exists between the onset of mood symptoms and a particular time of year, that is not due to seasonally-related situational stressors such as unemployment or the anniversary of a bereavement or trauma. The mood symptoms must remit or change (from depression to mania or hypomania or vice versa) at a particular time of year. There must have been recurrent temporally-related depressive episodes for 2 years, without any depressive episodes at other times, and seasonally-related depressive episodes must outnumber non-seasonal depressions over the patient’s previous lifetimes. The seasonal features may also be characterized as mild, moderate or severe, according to number of symptoms present, severity of symptoms and degree of functional impairment caused by symptoms. “Mild” seasonal exacerbations are characterized by enough symptoms to meet the criteria, distressing but manageable symptoms and minor functional impairment; more symptoms than required for diagnosis and more intense symptoms that cause social or occupational impairment constitute “moderate” severity and “severe” seasonal symptoms are numerous, intensely distressing and cause significant limitation or impairment. Symptoms may also be characterized as partially remitted (some symptoms from the last episode are present but do not meet diagnostic criteria, or symptoms have been remitted for 2 months or less) or in full remission (no symptoms for at least 2 months). The disorder can also be subsyndromal, with troublesome symptoms that are not numerous enough or do not last long enough to permit formal diagnosis.
Epidemiology
The epidemiology of seasonal affective disorder has been extensively studied, in order to determine whether geographical location and daylight length are pathogenetic factors (Magnusson & Partonen, 2005). These studies have generally used the Seasonal Pattern Assessment Questionnaire, which measures changes with season in mood, social activities, appetite, weight, sleep and energy (Rosenthal, Genhart, Sack, Skwerer & Wehr, 1987). The Seasonal Health Questionnaire has also been used to identify seasonal variation in mood disturbance (Blazer, Kessler & Swartz, 1998). Prevalence rates of 1 to 10 per cent have been recorded using these measures, with a preponderance of women and young adults. Subsyndromal seasonal affective disorder, the “winter blues”, occurs in 14 per cent of the U.S. population (Avery, Kizer, Bolte & Hellekson, 2001).
Prevalence rates are higher in North America than in Europe or the Southern Hemisphere, but on all continence prevalence is less in warmer and sunnier climates than in northern latitudes. Among outpatients followed for depression, 10 to 20 per cent meet criteria for seasonal affective disorder, and seasonality is more frequent with bipolar disorder than with major depressive disorder. About 4 per cent of children between 9 and 12 years of age met these criteria, with lower rates among younger children and in girls; 3 per cent of adolescents were found to have seasonal mood exacerbations, with initially equal representation of girls and boys but an increase after puberty and the emergence of female preponderance.
Seasonal affective disorder is often comorbid with other psychiatric disorders, particularly anxiety disorders, eating disorders, obsessive-compulsive disorder and substance abuse (now substance use disorders), particularly alcoholism. The comorbid disorders have not been shown to have seasonal exacerbations as the mood symptoms do.
Most studies have shown a latitude gradient for seasonal affective disorder, with increasing prevalence with more northerly latitude. This has not been found in southern Europe or Turkey, and evidence of a latitude gradient is less marked in the southern hemisphere, but seasonal symptoms increase from south to north in Japan, although the prevalence there is low. A correlation has also been found between seasonal affective disorder prevalence and hours of direct sunlight, degree of cloud cover and measures of solar irradiation. Iceland is a notable exception to the latitude gradient: despite its northerly location, seasonal affective disorder is less common in Iceland than in North America or Scandinavia. It has been suggested that the low prevalence in Iceland and Japan may be due to diets peculiarly high in fish in both countries. The lower prevalences may also reflect genetic factors, as Icelandic immigrants in Canada and Japanese living in Sweden also had lower rates of seasonal affective disorder. In contrast, Russians in Siberia had higher prevalence rates for seasonal affective disorder than the aboriginal inhabitants of Siberia, and seasonal affective disorder was much more common among Russians living on Svalbard in the Arctic Ocean, the northernmost permanently- inhabited place in the world, than among Norwegians living there.
Pathophysiology
An analogy has been suggested between the reduced activity, hypersomnolence and low mood of seasonal affective disorder and the hibernation seen in other species: both may represent an adaptive reduction in calorie intake and cessation of reproduction during the winter (Nesse & Williams, 1996). The depressive symptoms have been related to ambient light and are alleviated by an artificial increase in daylight, and these may be mediated by melatonin secretion by the pineal gland in response to dim light (Lam & Levitan, 2000). The symptoms are also consistent with decreased serotonin levels or effect, and the variable occurrence and severity could be due to genetic polymorphisms governing serotonin synthesis and transport (Johansson, Willeit, Levitan, Partonen, Smedh, del Favero, Bel Kaçem, Praschak-Rieder, Neumeister, Masellis, Basile, Zill, Bondy, Paunio, Kasper, Van Broeckhoven, Nilsson, Lam, Schalling & Adolfsson, 2003).
Treatment
The predominant treatment for seasonal affective disorder is light therapy. Antidepressants and occasionally other medications, ionized-air administration, melatonin supplementation and cognitive-behavioral psychotherapy have also been found to be effective. Physical exercise, with or without light therapy or other interventions, has also been found beneficial (Roecklein & Rohan, 2005).
Bright light is usually given with a light box as full-spectrum white light at 10,000 lux, blue light (480 nm wavelength) at 2,500 lux or blue-green light (500 nm wavelength) at 350 lux. The patient sits 30-60 cm from the light source with eyes open for 30-60 minutes. This is an effective regimen, but as many as 70 per cent have found it inconvenient and up to 19 per cent have discontinued phototherapy for this reason (Avery, Eder, Bolte, Hellekson, Dunner, Vitello & Prinz, 2001). Increased time outdoors or a computer-controlled heliostat to reflect sunlight into windows are also effective. The release of negative ions into the sleeping environment has produced up to 50 per cent improvement in seasonal symptoms (Terman, Terman & Ross, 2006).
SSRI antidepressants (fluoxetine, paroxetine and sertraline) have been shown to be effective for seasonal depression, and buproprion is an effective prophylactic at times of increased seasonal risk. Modafinil and vitamin D supplementation have been suggested on the basis of open label studies. These modalities are more effective when combined with light therapy (Lam, Levitt, Levitan, Enns, Morehouse, Michalak & Tan, 2006).
Seasonal affective disorder has been associated with negative thought patterns that are correlated with depression: automatic negative thoughts, a negative attributional style and dysfunctional assumptioms or attitudes. There is also a propensity to rumination in such individuals, and enjoyment of and participation in pleasant events decreases while negative responses to light-related stimuli increase at times of seasonal mood disturbance, particularly winter. Cognitive-behavioral psychotherapy is effective for negative thinking, rumination and disengagement from potentially pleasurable activities, and is an established therapy for major depressive disorder. Controlled trials have shown significantly greater amelioration and lower relapse rates with cognitive-behavioral therapy of seasonal depression, with and without concomitant light treatment (Rohan, Lindsey, Roecklin & Lacy, 2004).
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