Atypical depression was originally used to describe a subgroup of patients who responded relatively poorly to tricyclic antidepressants but robustly to monoamine oxidase inhibitors. The Colombia group has defined atypical depression as requiring mood ...
Atypical depression was originally used to describe a subgroup of patients who responded relatively poorly to tricyclic antidepressants but robustly to monoamine oxidase inhibitors. The Colombia group has defined atypical depression as requiring mood reactivity unlike melancholic type of depression. For a diagnosis of definite atypical depression, in addition to absense of typical endogenous features of depressive symptoms, two of four associated symptoms are required. These include ① hypersomnolence, ② hyperphasia,③leaden paralysis (intense lethality) and ④ pathologic sensitivity to interpersonal rejection. Although limited to data concerning clinical phenomenology and treatment response, the evidence concering the validity of atypical depression suggests that it is a unique subtype of depression. But the biological nature of atypical depression has been minimally investigated till now. Some of previous researches that investigated the sleep patterns, dichotic listening. brain evoked potentials and other neuroendocrine variables in patients with atypical depression suggested that these patients have a less severe biological dysfunctional noradrenergic system. However there is a increasing evidence that atypical depression is associated with a decreased central serotonergic activity and that treatment with serotonin potentiating drugs may result in therapeutic success. Central serotonin system participate in the regulation of mood and behavioral impulsivity, and modulating sleep and eating pattems qualitatively and quantitatively. Depressives with premenstrual syndromes and seasonal affective disorders, which are frequently accompanied by symptoms of atypical feature, in general, also benefit from treatments with serotonin potenitiating drugs, suggesting that brain serotonin plays a major role in the pathophysiology of atypical depression. Differential response to tricyclic antidepressants or monoamine oxidase inhobitors between major depressive with melancholia and those with atypical depression implies a difference in the biochemiostry of the two disorders. Comparison of biochemical variables between major depressive with melancholia whose symptoms are characterized by insomnia and loss of appetite vs those with atypical depression whose symptoms are characterized by hypersomnolence and increased appetite might be a fruitful avenue of future research.