Quand la saison devient synonyme de dépression

Abstract

Bien que les médecins et les psychiatres reconnaissent de plus en plus la réalité du trouble affectif saisonnier (TAS), l’étiologie de ce mal reste encore obscure. Tout ce qu’on peut affirmer à propos de cette pathologie, c’est l’existence d’un lien entre la baisse de luminosité ambiante à partir de l’automne puis au cours de l’hiver et l’apparition de symptômes dépressifs. Mais pourquoi cette diminution de luminosité rend-elle certaines personnes dépressives et pas d’autres ? Pourquoi et comment l’exposition au soleil peut-elle affecter la régulation de l’humeur par le cerveau ? Cet article propose de faire la lumière sur les principales hypothèses neurochimiques avancées au cours des vingt-cinq dernières années. Il souligne également l’importance de la mélatonine, de la sérotonine et des catécholamines dans la physiopathologie du TAS.

Although becoming more and more recognized among physicians and psychiatrists the etiology of seasonal affective disorder (SAD) remains unclear. Indeed, the only incontestable fact is the close link between the decrease in sunlight occurring during fall and winter and the onset of depressive symptoms. But why does this seasonal decrease in the amount of light trigger a depression in some individuals while not affecting others ? Why and how has sun exposure such an impact on brain-mood regulation ? This review intends to shed some light on the main neurochemical hypotheses that have been advanced for the past 25 years. While several hypotheses have been advanced to explain SAD, the present review will focus on three major suspects which are: (1) melatonin due to its crucial role in circadian rhythms (2) serotonin which has been linked with depressive disorders in general and atypical symptoms and (3) catecholamine because as for serotonin, many data reported an implication of these neurotransmitter family in depressive disorders. However, similarly to other reviews about SAD, we conclude that none of those could explain the pathophysiology of this northern disease on its own.