Objective: Our aim is to report three cases of orolingual dyskinesia in adults receiving intrathecal ziconotide for chronic pain management.

Background: Ziconotide (ZCN), a nonopioid analgesic, is first-line intrathecal therapy for patients with severe chronic pain refractory to other management options [1-2]. It is used to treat neuropathic pain because it inhibits nociceptive signal transmission in the spinal cord by selectively blocking presynaptic N-type voltage sensitive calcium channels of the dorsal horn [3]. Central nervous system-related side effects of ZCN infusions (hallucinations and psychosis) have been well described [4-6], but few reports exist of orofacial dyskinesias. We present three such cases associated with intrathecal ziconotide and posit why this therapy may produce hallucinations and dyskinesias in patients.

Method: 3 patients at our tertiary referral center experienced orolingual dyskinesia after initiating intrathecal ziconotide. Discontinuation of ZCN enabled resolution or marked improvement in the observed movement disorder.

Results: Case 1 is a 43-year-old man with a ZCN pump placed in March 2017 for painful diabetic neuropathy. After a good initial response, he developed oral dyskinesias and movements of his head and wrists. Discontinuing ZCN resolved orofacial dyskinesias, although tactical dysesthesias in his feet persist. Case 2 is a 70-year-old who experienced mental status changes and involuntary tongue movements after initiating ZCN therapy in 2015 for chronic neck pain. At the patient’s request, dosage was increased to improve pain control despite the persisting dyskinesias. Oral dyskinesias resolved after discontinuing ZCN due to worsening hallucinations. Case 3 is 64-year-old woman who began intrathecal ZCN in 2017 for chronic back pain and developed involuntary twitching of the lower face and tongue. Reducing, then discontinuing ZCN dosage improved but did not resolve the orofacial dyskinesias.

Conclusion: Given the temporal association with increased doses of ZCN, the near or complete resolution with ZCN discontinuation and similar location and movement disorder phenomenology in the 3 cases, the dyskinesias described are likely caused by intrathecal ZCN and dose-related in nature. These cases justify close monitoring of patients treated with ZCN for involuntary movements.  Since dyskinesia persisted in one of our patients after discontinuing ZCN, a chronic (tardive) movement disorder may also be a risk with ZCN.

References: [1] Hassen Busch SJ., Portenoy RK. Current practices in intraspinal therapy: a survey of clinical trends and decision making. J Pain Symptom Manage 2000;20:S4–S11. [2] Hassenbusch SJ., Portenoy RK., Cousins M et al. Polyanalgesic Consensus Conference 2003: an update on the management of pain by intraspinal drug delivery—report of an expert panel. J Pain Symptom Manage 2004;27:540–563. [3] Miljanich G. Ziconotide: neuronal calcium channel blocker for treating severe chronic pain. Curr Med Chem. 2004;11(23):3029–40. [4] Burdge, G., Leach, H., & Walsh, K. (2018). Ziconotide-induced psychosis: A case report and literature review. Mental Health Clinician, 8(5), 242-246. [5] Phan, S. V., & Waldfogel, J. M. (2015). Ziconotide-induced psychosis: a case report. General hospital psychiatry, 37(1), 97-e11. [6] Whitlow J., Mu K., Coverdale J., Shah A. Ziconotide-associated psychosis treated with Invega. Psychiatric Ann. 2015;45(2):64–6.

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