Pharmacology mirtazapine

Nutt D. (1997). Mirtazapine pharmacology in relation to adverse effects. Acta Psychiatr Scand. SuppI 391 31-37. 

Pharmacology Tetracyclics enhance central noradrenergic and serotonergic activity. They do not inhibit monoamine oxidase. Although maprotiline and mirtazapine are in the same chemical class, they each affect different neurotransmitters and thus have different side effect profiles. Maprotiline primarily acts by blocking reuptake of norepinephrine at nerve endings. 

AnttilaSA, Leinonen EV. A review of the pharmacological and clinical proHle of mirtazapine. CNS Drug Rev 200i 7 249-264. 

Treatment of GAD can be undertaken using a number of pharmacological agents. Benzodiazepines have been found to be superior to placebo in several studies and all benzodiazepines appear to be equally effective. However, side effects include sedation, psvchomotor impairment, amnesia and tolerance (Chapter 1). Recent clinical data indicate that SSRIs and SNRIs are effective in the treatment of acute GAD symptoms. Venlafaxine, paroxetine and imipramine have been shown to be effective antianxiety medications in placebo-controlled studies. Case studies also indicate the usefulness of clomipramine, nefazodone, mirtazapine, fluoxetine and fluvoxamine in GAD. Buspirone, a 5-HTla receptor partial agonist, has been shown to be effective in several placebo-controlled, double-blind trials (Roy-Byme and Cowley, 2002). Buspirone has a later onset of action than both benzodiazepines and SSRIs but with the advantage of being non-addictive and non-sedating. 

Mirtazapine has a complex pharmacology. It is an antagonist of the presynaptic k2 autoreceptor and enhances the release of both norepinephrine and 5-HT. In addition, mirtazapine is an antagonist of 5-HT and 5-HT receptors. Finally,... 

The time spent reviewing the pharmacology of venlafaxine, mirtazapine and nefazodone was just right. ... 

Pharmacological treatment of OSA is an elusive concept. A number of selective serotonin receptor inhibitors (SSRIs) and other medications were tried and found to be ineffective. SSRIs and analogous medication have been anecdotally reported to help REM-related OSA, but no study systematically confirmed this claim. Two studies showed positive effect of mirtazapine [33, 34], a tetracyclic non-SSRI antidepressant, on OSA, but further research on a bigger sample is necessary. On the other hand, one should be aware of a muscle relaxation property of some commonly used medications such as benzodiazepines (BZDs), which may result in a worsening of OSA. Assisted nasal ventilation is commonly used in patients with both hypercapnic and non-hypercapnic CSA. The administration of oxygen is observed to ameliorate the frequency of both the central and obstructive events in patients with a predomi-... 

Subsequently, the UK Committee on Safety of Medicines issued guidance for practitioners, indicating that with the exception of fluoxetine, the benefit-harm balance of SSRIs and venlafaxine in depressed children and adolescents was unfavorable (27). A similar conclusion was drawn concerning mirtazapine. It is, however, puzzling that the therapeutic effects of fluoxetine should be quite so different from compounds that are similar pharmacologically. One important issue might be the relevance of regulatory trials of antidepressants to real-world treatment. Placebo-controlled trials in depression... 

In patients who do not respond to SSRI treatment, the addition of mirtazapine is an increasingly popular option. Mirtazapine is an a2-adrenoceptor antagonist, so its acute pharmacological effects predominantly involve potentiation of noradrenergic function. This might be expected to enhance the serotonergic actions of SSRIs. 

The antidepressant mirtazapine is pharmacologically similar to mianserin. It has a slightly weaker blocking action at i-adrenoceptors, and this is claimed to give it a dual mode of action, increasing the release of both noradrenaline and serotonin (1). It is claimed to have a more rapid onset of action than some SSRIs, but this may be due to its prominent sedative effect, which improves insomnia from the start of treatment. 

Unlike most other antidepressants, mirtazapine does not inhibit the reuptake of monoamines, but instead blocks inhibitory a2-adrenoceptors. It is conceivable that this pharmacological mechanism led to hypomanic symptoms in this patient. 

Allison, D. B. and D. E. Casey (2001). Antipsychotic-induced weight gain a review of the literature. J Clin Psychiatry 62(Suppl 7) 22-31. Anttila, S. A. and E. V. Leinonen (2001). A review of the pharmacological and clinical profile of mirtazapine. CNS Drug Rev 7(3) 249-64. Baptista, T., N. M. Kin, S. Beaulieu and E. A. de Baptista (2002). Obesity and related metabolic abnormalities during antipsychotic drug administration mechanisms, management and research perspectives. Pharmacopsychiatry. 35(6) 205-19. 

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