Objective: To describe the case of a parkinsonian patient treated by apomorphine pump who stopped smoking without difficulty despite being dependent to nicotine. To explore possible links between apomorphine and smoking cessation.

Background: A 52-year old Caucasian female with idiopathic Parkinson’s disease (PD, disease duration = 14 years) was offered initiation of continuous subcutaneous apomorphine infusion (CSAI) in 2015. Her medical history revealed that she started smoking at 19. She had previously tried to stop smoking using nicotine replacement at the age of 30 and 38 (followed by relapse) and had cut down her smoking during her two pregnancies, with difficulty. After hearing her PD diagnosis in 2008, she increased her cigarette consumption. At the time of the evaluation, she was a daily smoker (mean of 20 cigarettes per day) and the Fagerström Test for Nicotine Dependence (FTND) yielded a score of 8 (range: 0-10), reflecting a high dependence to nicotine.

Method: Case Report and Literature Review.

Results: Motivated by economic reasons, the patient decided to try again to stop smoking, using a smoking cessation app. Her medications at the time were as follow: levodopa 400mg/day with benserazide 100mg/day, duloxetine 60mg/day, levothyroxine 25 μg/day, and CSAI 3,5mg/hr for 14hr and 3mg/hr for 6 hr (with occasional boluses as needed). To her great surprise, the patient stopped smoking overnight without difficulty and without recurring to nicotine replacement therapies. She spontaneously reported the absence of tobacco withdrawal symptoms and the emergence of disgust for the smell of cigarette to her neurologist (CG). She smoked one cigarette in a festive context, but reported no pleasure and no craving. The patient has since completely stopped smoking (30 days).

Conclusion: Although the patient’s abstinence will have to be reassessed during her neurological follow-up, this case-report adds to the existing literature on the possible links between apomorphine administration and smoking cessation [1,2,3]. Neuromolecular evidence [2,3] suggest that apomorphine could play a role in treating tobacco use disorder through dopamine and serotonergic pathways, possibly correcting signaling modifications induced by chronic nicotine exposure. Prospective clinical research is needed to fully assess apomorphine potential for smoking cessation.

References: [1] Stern G. Apolaustic apomorphine. Pract Neurol. 2013 Oct;13(5):335-7. [2] Morales-Rosado JA, Cousin MA, Ebbert JO, Klee EW. A Critical Review of Repurposing Apomorphine for Smoking Cessation.Assay Drug Dev Technol. 2015 Dec;13(10):612-22. [3] Cousin MA, Ebbert JO, Wiinamaki AR, Urban MD, Argue DP, Ekker SC, Klee EW. Larval Zebrafish Model for FDA-Approved Drug Repositioning for Tobacco Dependence Treatment. PLoS One. 2014; 9(3): e90467.

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