The Diagnosis, Symptomatology, and Epidemiology of Seasonal Affective Disorder

CNS Spectrums ◽  
2005 ◽  
Vol 10 (8) ◽  
pp. 625-634 ◽  
Author(s):  
Andres Magnusson ◽  
Timo Partonen

AbstractThe 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.

2018 ◽  
Vol 52 (12) ◽  
pp. 1173-1182 ◽  
Author(s):  
Gordon Parker ◽  
Gabriela Tavella ◽  
Glenda Macqueen ◽  
Michael Berk ◽  
Heinz Grunze ◽  
...  

Objective: To derive new criteria sets for defining manic and hypomanic episodes (and thus for defining the bipolar I and II disorders), an international Task Force was assembled and termed AREDOC reflecting its role of Assessment, Revision and Evaluation of DSM and other Operational Criteria. This paper reports on the first phase of its deliberations and interim criteria recommendations. Method: The first stage of the process consisted of reviewing Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, and recent International Classification of Diseases criteria, identifying their limitations and generating modified criteria sets for further in-depth consideration. Task Force members responded to recommendations for modifying criteria and from these the most problematic issues were identified. Results: Principal issues focussed on by Task Force members were how best to differentiate mania and hypomania, how to judge ‘impairment’ (both in and of itself and allowing that functioning may sometimes improve during hypomanic episodes) and concern that rejecting some criteria (e.g. an imposed duration period) might risk false-positive diagnoses of the bipolar disorders. Conclusion: This first-stage report summarises the clinical opinions of international experts in the diagnosis and management of the bipolar disorders, allowing readers to contemplate diagnostic parameters that may influence their clinical decisions. The findings meaningfully inform subsequent Task Force stages (involving a further commentary stage followed by an empirical study) that are expected to generate improved symptom criteria for diagnosing the bipolar I and II disorders with greater precision and to clarify whether they differ dimensionally or categorically.


1995 ◽  
Vol 7 (3) ◽  
pp. 75-79
Author(s):  
J. Beullens

SummaryMelatonin is a hormone secreted by the pineal gland mainly during the night. The discovery that this melatonin secretion decreases under the influence of bright light, gave rise to the use of light therapy in some affective disorders. The literature on the relationship between melatonin secretion and mood is reviewed concerning seasonal affective disorder, non-seasonal affective disorder and premenstrual syndrome. Light therapy could reduce an abnormal high melatonin secretion back to normal proportions. None of the affective disorders, however, is accompanied by an unusual high melatonin level. Nevertheless, light therapy as well as other therapies that suppress melatonin have a therapeutic effect. This is not the case with the administration of melatonin. Mood is not affected by extra melatonin in seasonal affective disorder but it is in both other affective disorders. Melatonin plays a part in the pathogenesis of the affective disorders but it is not yet clear which one.


2003 ◽  
Vol 13 ◽  
pp. S247-S248
Author(s):  
E. Pjrek ◽  
D. Winkler ◽  
A. Konstantinidis ◽  
N. Thierry ◽  
A. Heiden ◽  
...  

2011 ◽  
Vol 26 (S2) ◽  
pp. 247-247
Author(s):  
M. Schmoeger ◽  
S. Cohen-Woods ◽  
G. Hosang ◽  
M. Schloegelhofer ◽  
I. Craig ◽  
...  

According to Oedegaard et al. (2010) the co-morbidity of migraine and bipolar disorder (BPD) is well documented in numerous epidemiological and clinical studies, and there are clear pathophysiological similarities. Interestingly, in a genome-wide scan, Lea et al. (2005) identified a susceptibility locus for a severe heritable form of common migraine on chromosome 3q29. With respect to BPD, a susceptibility region on chromosome 3q29 was identified in a genome-wide linkage scan (Bailer et al. 2002) and follow-up linkage analysis (Schosser et al. 2004). These findings were also supported by further fine-mapping of this region (Schosser et al. 2007). Since 3q29 is among the chromosomal regions implicated in migraine and bipolar linkage studies, the aim of the current study is to test for 3q29 association of migraine in sample of patients with BPD. The sample consists of 463 patients with a diagnosis of BPD (34.63% men, 65.37% women; mean age ± SD: 48.01 ± 11.26), as defined by the Diagnostic and Statistical Manual 4th edition operational criteria (DSM-IV) and the International Classification of Diseases 10th edition operational criteria (ICD-10), derived from the Bipolar Affective Disorder Case Control Study (BACCS). A total of 51 SNPs in the region of the 3q29 were genotyped using Sequenom MassARRAY® iPLEX Gold and tested for association with migraine. The results of this association study investigating the 3q29 region in a sample of patients with BPD will be presented.


2000 ◽  
Vol 30 (1) ◽  
pp. 79-87 ◽  
Author(s):  
R. W. LAM ◽  
T. A. BOWERING ◽  
E. M. TAM ◽  
A. GREWAL ◽  
L. N. YATHAM ◽  
...  

Background. Serotonergic mechanisms have been proposed for the pathophysiology of seasonal affective disorder (SAD) and the therapeutic effect of bright-light treatment. Previously, we showed that SAD patients, in clinical remission with light therapy during the winter, experienced transient depressive relapses after a rapid tryptophan depletion (RTD) technique, which results in decreased brain serotonin levels. The objective of this study was to investigate the effect of RTD in SAD patients who were in natural summer remission.Methods. Twelve drug-free patients with SAD by DSM-IV criteria and 10 normal subjects participated in this double-blind, placebo-controlled, crossover study. SAD patients were in natural summer remission for at least 8 weeks. Behavioural ratings and plasma tryptophan levels were obtained before, and 5 h after, ingesting an amino acid (AA) mixture±tryptophan. Experimental RTD and control sessions were scheduled 1 week apart.Results. The RTD session resulted in significant reduction in total and free plasma tryptophan levels compared to the control session. The behavioural data were analysed using repeated measures analysis of variance. This analysis found significant main effects of time (higher scores after AA ingestion) and diagnosis (higher scores in SAD patients), but no main effect of session or significant interaction effects between the three factors. Thus, there were no significant behavioural effects of RTD compared to the sham depletion control session.Conclusions. The summer remission experienced by SAD patients is not dependent on plasma tryptophan levels (and presumably brain serotonin function) in the same manner as that of remission after light therapy. These results conflict with those of other laboratories, perhaps because of differences in study samples.


1995 ◽  
Vol 119 (2) ◽  
pp. 202-210 ◽  
Author(s):  
PAMELA F. GALLIN ◽  
MICHAEL TERMAN ◽  
CHARLOTTE E. REMÉ ◽  
BRIAN RAFFERTY ◽  
JIUAN SU TERMAN ◽  
...  

Author(s):  
Kelly Rohan ◽  
Jennifer N. Rough

Winter seasonal affective disorder (SAD) is a subtype of depression, characterized by the recurrence of major depressive episodes in the fall and/or winter months. In North America, SAD prevalence and severity are inversely related to photoperiod, such that SAD is more common at northern latitudes. Photoperiod is the most robust environmental predictor of SAD episode onset. Research has supported a potential role for both physiological and psychological vulnerabilities in the development and maintenance of SAD. Specifically, SAD has been linked to abnormal circadian functioning, retinal sensitivities to low light availability, and maladaptive cognitive and behavioral responses in winter. SAD symptoms can be comparably and effectively treated with different modalities including light therapy, antidepressants, and cognitive–behavioral therapy. Future research should continue to explore and integrate different vulnerabilities as a means to further refine effective treatment and prevention efforts.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Marie Spies ◽  
Gregory M. James ◽  
Chrysoula Vraka ◽  
Cécile Philippe ◽  
Marius Hienert ◽  
...  

1995 ◽  
Vol 40 (8) ◽  
pp. 457-466 ◽  
Author(s):  
Edwin M Tam ◽  
Raymond W Lam ◽  
Anthony J Levitt

Objective To review the status of current treatment of seasonal affective disorder (SAD). Method Treatment studies of SAD published between January 1989 and March 1995 were identified using a computerized MEDLINE literature search. Additional citations were obtained from the reference sections of these articles. Studies included in this review were selected using operational methodologic criteria. Results Many studies support the efficacy of bright light therapy using a fluorescent light box. The best studied protocol is >2500 lux white light for 2 hours per day, but newer protocols using 10,000 lux for 30 minutes have comparable response rates. Studies of light visors and other head-mounted devices also report similar response rates, but have not yet shown superiority over putative control conditions. There are fewer medication studies in SAD, but controlled studies suggest that fluoxetine, d-fenfluramine and propranolol are effective. Other treatments such as dawn simulation require further study. No studies of psychological treatments for SAD were found. Many studies had methodologic limitations, including brief treatment periods, small sample sizes, and lack of replication, that limit the generalizability of findings. Conclusion There are several well-studied, effective treatments for SAD, including light therapy and medications. However, further research must be done to demonstrate sustained treatment response over time, to clarify the intensity-response relationship of light therapy, to clarify the role of light therapy and medications, and to assess combination treatments.


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