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Neurology India, Vol. 58, No. 4, July-August, 2010, pp. 672-673 Letter To Editor Gradual onset of dyskinesia induced by mirtazapine Balaz Marek, Rektor Ivan Movement Disorders Center, Department of Neurology, St. Anne's University Hospital, Medical School of Masaryk University, Pekarska 53, 656 91 Brno, Czech Republic Correspondence Address:Movement Disorders Center, Department of Neurology, St. Anne's University Hospital, Medical School of Masaryk University, Pekarska 53, 656 91 Brno, Czech Republic, marek.balaz@fnusa.cz Date of Acceptance: 21-Jul-2010 Code Number: ni10182 PMID: 20739826 DOI: 10.4103/0028-3886.68693 Sir, Mirtazapine is a noradrenergic and specific serotonergic antidepressant (NaSSA) and is approved for the treatment of major depressive disorder and also has the potential to be of use in other psychiatric disorders. [1] Cases of acute onset dyskinesia, [2] dystonia, [3] and akathisia [4] have been reported with mirtazapine treatment. In this report, we present a patient who developed gradual onset of dyskinesia on mirtazapine. A 76-year-old woman was diagnosed with depression and anxiety disorder in December 2006 and was put on clonazepam with a positive effect on anxiety symptoms; however she discontinued the medication. In September 2007, mirtazapine (15 mg/day) was added. On 26 October 2007, her general practitioner noted "flared" movements of her limbs. One month later, the patient noticed fidgeting finger movements and involuntary movement in her left lower limb. In February 2009, she was admitted to the neurology ward of a regional hospital for the evaluation of the movement disorder. Her previous medical history was unremarkable, and she had no family history of any neurological or psychiatric disorders. Extensive laboratory screening, including T1 and T2 magnetic resonance imaging, 99mTc-hexamethyl propylene-amine oxime single photon emission computed tomography (HMPAO SPECT), hematological and biochemical tests (including a blood smear for acanthocytes), and genetic testing for Huntington′s disease, failed to provide any identifiable etiology. With tiapridal (600 mg/day) there was a mild improvement in the dyskinesia. After several months, the dose was tapered to 400 mg/day with no change in the patient′s condition. She was later referred to our Movement Disorders Center. The patient presented with repeated perioral and tongue dyskinesia and dyskinesia of the left lower limb. Movements were of moderate intensity, and the patient was aware of them. There were no other significant neurological findings. Mirtazapine was discontinued, and the patient was referred to her psychiatrist with a recommendation to change her antidepressant medication. After 2 months, the patient returned to our clinic with improvement in her symptoms: only mild perioral dyskinesia and no lower limb dyskinesia. The decrease in symptoms was gradual, with most of the improvement occurring in the first 2 weeks. The family member who accompanied the patient at both visits also noted a major improvement in the patient′s physical state. We believe this patient is probably the first case of gradual onset dyskinesia with mirtazapine treatment. Mirtazapine has been suggested for treating antipsychotic-induced akathisia. [5] Earlier reports [2],[4] and also our patient suggest that one should be observant while treating patients with mirtazapine for the development of dyskinesia or worsening of akathisia. We agree with Kumar et al. [6] that one should be aware that antidepressant medications can cause various movement disorders. The possible mechanism for dyskinesia may be mediated by the 5-HT2 receptors. 5-HT2 antagonists have been shown to have some activity to promote motor function in states of reduced dopamine release. [7] Mirtazapine has been shown to be effective in treating resting tremor in patients with Parkinson′s disease. [8] However, the exact mechanism of mirtazapine-induced dystonia seems to be unclear. [9] Mirtazapine could have a broader biochemical spectrum rather than a narrow effect on serotonin or it could also have binding sites in the basal ganglia output structures. [10] References
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