Chronic Serotonergic Overstimulation Mimicking Panic Attacks in a Patient with Parkinson’s Disease Receiving Additional Antidepressant Treatment with Moclobemide

Author:

Praetner Marc1ORCID,Schiele Timo2ORCID,Werle Lukas3ORCID,Kuffer Janina4ORCID,Nischwitz Sandra5ORCID,Keck Martin E.6ORCID,Kloiber Stefan578ORCID

Affiliation:

1. Walter Brendel Center of Experimental Medicine, Ludwig-Maximilians-Universität München, Marchioninistr. 15, 81377 Munich, Germany

2. Psychosomatische Klinik Kloster Dießen GmbH & Co. KG, Klosterhof 20, 86911 Dießen am Ammersee, Germany

3. Benedictus Krankenhaus Tutzing Bahnhofstraße 5, 82327 Tutzing, Germany

4. Algesiologikum GmbH, Heßstr. 22, 80799 Munich, Germany

5. Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany

6. Kliniken Schmieder 78260 Gailingen am Hochrhein, Germany

7. Department of Psychiatry, University of Toronto, Canada

8. Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, 100 Stokes Street, Toronto, ON M6J1H4, Canada

Abstract

Background. The pharmacological treatment options of Parkinson’s disease (PD) have considerably evolved during the last decades. However, therapeutic regimes are complicated due to individual differences in disease progression as well as the occurrence of complex nonmotor impairments such as mood and anxiety disorders. Antidepressants in particular are commonly prescribed for the treatment of depressive symptoms and anxiety in PD. Case Presentation. In this case report, we describe a case of a 62-year-old female patient with PD and history of depressive symptoms for which she had been treated with moclobemide concurrent with anti-Parkinson medications pramipexole, rasagiline, and L-DOPA+benserazide retard. An increase in the dosage of moclobemide 12 months prior to admission progressively led to serotonergic overstimulation and psychovegetative exacerbations mimicking the clinical picture of an anxiety spectrum disorder. After moclobemide and rasagiline were discontinued based on the hypothesis of serotonergic overstimulation, the patient’s psychovegetative symptoms subsided. Conclusions. The specific pharmacological regime in this case probably caused drug-drug interactions resulting in a plethora of psychovegetative symptoms. Likely due to the delayed onset of adverse effects, physicians had difficulties in determining the pharmacologically induced serotonin toxicity. This case report emphasizes the complexity of pharmacological treatments and the importance of drug-drug interaction awareness in the treatment of PD patients with complicating nonmotor dysfunctions such as depression.

Publisher

Hindawi Limited

Subject

Psychiatry and Mental health

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