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Reversible extrapontine and central pontine myelinolysis presenting with extrapyramidal features

โœ Scribed by Bryan Ho; Diana Apetauerova; Christine Thomas; Jeffrey Arle; James A. Russell


Publisher
John Wiley and Sons
Year
2006
Tongue
English
Weight
71 KB
Volume
21
Category
Article
ISSN
0885-3185

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โœฆ Synopsis


thyroid stimulating hormone was negative. There was no family history of neurological or movement disorder.

The patient reported an overall improvement in his energy level and mood on the bupropion. However, he continued to complain of insomnia, poor concentration, and anxiety. Mirtazapine was added as augmentation for treatment of his residual insomnia, anxiety, and depressive symptoms. Shortly after the addition of mirtazapine at a dose of 15 mg/day, it was noted that his dyskinesia decreased in frequency and intensity. With further titration of the mirtazapine to 45 mg/day over the course of 4 weeks, the orofacial movements were no longer present.

Bupropion is a novel antidepressant that has been postulated to function via dopaminergic pathways. There is a case report in the literature of buproprion-induced dyskinesia that reversed after discontinuation of the medication. 1 The mechanism of action whereby buproprion induces dyskinesia may involve dopamine reuptake inhibition and the enhancement of norepinephrine functional activity. 2 Mirtazapine is a novel antidepressant that disinhibits serotonergic and noradrenergic neurons by acting as an โฃ-2 antagonist. It also acts as a 5HT-2 and 5HT-3 antagonist and 5HT-1A agonist. 3 Drugs with 5HT-1A agonistic activity (such as buspirone) and with 5HT-2 antagonistic activity (such as ritanserin) have been reported to be effective in reducing L-dopa-induced dyskinesia. 4,5 There have also been case reports of mirtazapine being used to treat tremor and L-dopa-induced dyskinesia. 6 A literature search revealed no case reports or studies of using mirtazapine to treat bupropion-induced dyskinesia.

Patient management concerns did not allow us to explore direct causal relationships between bupropion and dyskinesias, or between mirtazapine and abatement of dyskinesias. Strict pharmacological testing would have included sequential withdrawal and reintroduction of the drugs to establish their specific roles. Nonetheless, to our knowledge, this case report is the first one to suggest that mirtazapine may be useful for the treatment of bupropion-induced dyskinesia in a similar manner to its reported efficacy in L-dopa-induced dyskinesia.


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