Melatonine en stemmingsstoornissen

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.

CNS Spectrums ◽  
2001 ◽  
Vol 6 (6) ◽  
pp. 487-501 ◽  
Author(s):  
Paul H. Desan ◽  
Dan A. Oren

AbstractSeasonal affective disorder (SAD) is a form of depression that starts in the fall and ends in the spring. This article reviews existing theories about the relationship between circadian rhythms and the disorder. Recent research indicates that as with pharmacologic antidepressants, at least 2–4 weeks are needed to demonstrate the effectiveness of bright-light therapy compared to placebo. The response to such treatment is strongest with precisely timed light exposure: treatment is optimal during the morning hours when the circadian systemt is susceptible to phase advance. Such clinical improvement is correlated with the magnitude of the phase shift induced. These observations suggest a model of circadian function in SAD and provide important guidelines for its treatment.


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.


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

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 ◽  
...  

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.


2021 ◽  
Vol 14 (1) ◽  
pp. dmm047217
Author(s):  
Anusha Shankar ◽  
Cory T. Williams

ABSTRACTThe development of animal models is a critical step for exploring the underlying pathophysiological mechanisms of major affective disorders and for evaluating potential therapeutic approaches. Although most neuropsychiatric research is performed on nocturnal rodents, differences in how diurnal and nocturnal animals respond to changing photoperiods, combined with a possible link between circadian rhythm disruption and affective disorders, has led to a call for the development of diurnal animal models. The need for diurnal models is most clear for seasonal affective disorder (SAD), a widespread recurrent depressive disorder that is linked to exposure to short photoperiods. Here, we briefly review what is known regarding the etiology of SAD and then examine progress in developing appropriate diurnal rodent models. Although circadian disruption is often invoked as a key contributor to SAD, a mechanistic understanding of how misalignment between endogenous circadian physiology and daily environmental rhythms affects mood is lacking. Diurnal rodents show promise as models of SAD, as changes in affective-like behaviors are induced in response to short photoperiods or dim-light conditions, and symptoms can be ameliorated by brief exposure to intervals of bright light coincident with activity onset. One exciting avenue of research involves the orexinergic system, which regulates functions that are disturbed in SAD, including sleep cycles, the reward system, feeding behavior, monoaminergic neurotransmission and hippocampal neurogenesis. However, although diurnal models make intuitive sense for the study of SAD and are more likely to mimic circadian disruption, their utility is currently hampered by a lack of genomic resources needed for the molecular interrogation of potential mechanisms.


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