Indirect α1 adrenoceptor-mediated enhancement of serotonin cell firing and direct blockade of inhibitory α2 heteroreceptors located on serotonin terminals are held responsible for the increase in extracellular serotonin. Because of this, mirtazapine has been said to be a functional "indirect agonist" of the 5-HT1A receptor. Increased activation of the central 5-HT1A receptor is thought to be a major mediator of efficacy of most antidepressant drugs. 5-HT2 receptor
Antagonism of the 5-HT2 subfamily of receptors and inverse agonism of the 5-HT2C receptor appears to be in part responsible for mirtazapines efficacy in the treatment of depressive states. Mirtazapine increases dopamine release in the prefrontal cortex. Accordingly, it was shown that by blocking the α2-adrenergic receptors and 5-HT2C receptors mirtazapine disinhibited dopamine and norepinephrine activity in these areas in rats. In addition, mirtazapines antagonism of 5-HT2A receptors has beneficial effects on anxiety, sleep and appetite, as well as sexual function regarding the latter receptor. Mirtazapine has been shown to lower drug seeking behaviour (more specifically to methamphetamine) in various human and animal studies. It is also being investigated in substance abuse disorders to reduce withdrawal effects and improve remission rates.Mirtazapine significantly improves pre-existing symptoms of nausea, vomiting, diarrhea, and irritable bowel syndrome in affected individuals. Mirtazapine may be used as an inexpensive antiemetic alternative to Ondansetron. In conjunction with substance abuse counseling, mirtazapine has been investigated for the purpose of reducing methamphetamine use in dependent individuals with success.
This surgical procedure introduces a shim between the inner wall of the larynx and the soft tissue supporting the vocal fold. As a result, the paralyzed vocal fold is supported in a position closer to the midline of the glottis, and retains its ability to vibrate and phonate efficiently.In addition to medialization thyroplasty, arytenoid adduction can be performed to improve phonation results. This medical procedure consists of pulling the vocal processes of the arytenoid medially while monitoring the voicing quality being produced by the patient. When the best phonation appears to be achieved, the vocal processes are then maintained in place by a thread.A further surgical intervention used to mitigate vocal fold paresis is laryngeal reinnervation. This procedure restores nerve supply to the larynx and can be accomplished according to different techniques. Depending on the specific condition (i.e. bilateral versus unilateral vocal fold paralysis), these techniques include reconnecting parts of the RLN, supplying the laryngeal muscles with a donor nerve like the ansa cervicalis, or connecting the RLN to a donor nerve. Post-surgical outcomes
In many cases, the surgical treatment options described above (temporary injection medialization, medialization thyroplasty, arytenoid adduction, and laryngeal reinnervation) have led to favourable outcomes as measured perceptually, acoustically, by laryngoscope, or via quality of life measures. However, none of these surgical interventions has been shown to be significantly better than the others. Voice therapy after surgery
It is generally recommended that voice therapy start 1 to 2 months after surgery, when swelling has subsided.