Mirtazapine: clinical overview
by
Gorman JM
Department of Psychiatry,
Columbia University, New York, NY 10032, USA.
J Clin Psychiatry 1999; 60 Suppl 17:9-13; discussion 46-8


ABSTRACT

There is currently available evidence that suggests that drugs combining 2 synergistic mechanisms of action (e.g., enhancement of both noradrenergic and serotonergic neurotransmission) may yield superior therapeutic efficacy compared with a single therapeutic mechanism of highly selective agents such as selective serotonin reuptake inhibitors (SSRIs). The differences in antidepressant efficacy favoring dual-acting drugs may exist in particular for 3 difficult-to-treat groups of patients: those with endogenous depression, those with severe depression, or hospitalized depressed patients. Mirtazapine differs from other new dual-acting antidepressants by not being a reuptake inhibitor. Its antidepressant activity may be related to a direct enhancement of noradrenergic neurotransmission by blockade of alpha2-autoreceptors. The rapid increase in serotonin (5-HT) synaptic levels by blockade of alpha2-heteroreceptors indirectly enhances 5-HT1A-mediated neurotransmission since 5-HT2 and 5-HT3 are blocked by mirtazapine. The antidepressant efficacy of mirtazapine was established in several placebo-controlled trials. Currently available evidence suggests that mirtazapine is effective in all levels of severity of depressive illness, as well as is in a broad range of symptoms associated with depression.
SSRIs
5-HT1a
Options
Mirtazapine
Nefazodone
Antidepressants
Alpha2 antagonism
Mirtazapine v SSRIs
Mirtazapine and memory
Mirtazapine v imipramine
Mirtazapine: clinical profile
Mirtazapine and depression
Antidepressant mechanisms
Mirtazapine and the receptors
Mirtazapine: pharmacokinetics
Mirtazapine: adverse side-effects
Mirtazapine-induced dysphoric mania
Mirtazapine: GH, prolactin, and cortisol secretion
Does early improvement predict later stable response?



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