Using of rtms and antidepressant drugs simultaneously to increase the therapeutic efficacy for patients with psychotic depression Paper

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Psychotic depression is a fairly common psychiatric condition that has been found to occur in nearly 20% of patients with major depression (Flores et al., 2006). The preferred treatment for psychotic depression so far has consisted of tricyclic antidepressants (TCAs) as also neuroleptic and electroconvulsive therapies (O’Neal et al., 2000). Patients with psychotic depression have a more severely disordered hypothalamic-pituitary-adrenocortical (HPA) axis (Kathol et al., 1989). The psychotic features of psychotic depression have been attributed also to excessive glucocorticoid activity (Schatzberg et al., 1985). Interestingly, HPA axis activity is, to a large extent, regulated by the combination of mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) (Spencer et al.

, 1998. Young et al., 2003). Any mismatch between them could lead to inappropriate responses to stress, and incidence of major depression (Young et al., 2003). Decreases in MR sensitivity postulated to occur in major depression could result in elevated cortisol levels (Gesing et al., 2001. Young et al., 2003). In contrast, GR gives rise to feedback modifications in response to rising levels of cortisol as, for example, in response to stress or following the circadian rhythm. Hence, a GR antagonist e.g., the anti-progesterone steroid mifepristone (dimethylaminophenyl (17(-hydroxy-11(1(4-dimethylaminophenyl) 17(1- propynyl)estra-4,9-dien-3-one) exerts a powerful effect in the rising section of the HPA axis (Flores et al., 2006). A major effect of mifepristone occurs through obstruction of GR in crucial regions of the brain and in monaminergic nuclei, thereby, directly leading to recovery of symptomatic and cognitive faculties.

First observed by Bickford et al.