Case report
Using STN DBS and medication reduction as a strategy to treat pathological gambling in Parkinson's disease

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Abstract

We describe two patients with Parkinson's disease (PD) who developed clinical criteria of pathological gambling addiction in the setting of increased dopamine replacement therapy (levodopa and dopamine agonist medications). The second patient showed also signs of dopamine dysregulation syndrome, with an addiction to dopaminergic medication. Neither patients responded to the standard therapy for gambling behavior, but dramatically improved after bilateral subthalamic nucleus (STN) deep brain stimulation (DBS) and early postoperative withdrawal of dopaminergic therapy. The possible therapeutic role of subthalamic nucleus deep brain stimulation (STN-DBS) on such a disabling behavior needs to be investigated prospectively.

Introduction

According to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) [1], pathological gambling is an impulse-control disorder, which is part of an obsessive–compulsive clinical spectrum. This behavioral disorder has a lifetime prevalence of 1.6% in the general population [2] and is characterized by a failure to resist the impulse to gamble despite several personal and financial consequences. In the recent years, an increasing number of Parkinson's disease (PD) patients with pathological gambling have been described (for a review see [3]). This report describes two PD patients whose pathological gambling developed with increased dopaminergic therapy and resolved after subthalamic nucleus deep brain stimulation (STN-DBS) and dosage reduction.

Section snippets

Case reports

Patient No. 1: A 43-year-old man developed PD at the age of 39, with tremor of the right hand and mild rigidity of the right leg. Family and personal history was negative for psychiatric disorders. His parkinsonian symptoms, predominantly rigid-akinetic, rapidly progressed over the next 2 years. He was given ropinirole (15 mg/day) with only a minimal response. Therapy was changed to pramipexole (2.1 mg/day) and levodopa (300 mg/day)/benserazide. Levodopa and pramipexole were then increased up to

Discussion

The pathogenesis of pathological gambling is not known with certainty, but neurotransmitter disturbances, particularly dopamine, have been shown to be involved. It has recently been reported that a dysfunction in the dopaminergic mesolimbic reward system might result in gambling and other addictive behavior [4]. Although an incidental comorbidity cannot be excluded, the existence of a connection between PD and pathological gambling appears to be reasonable.

The gambling behavior of our PD

Acknowledgments

We thank Jeanne Tasker for the English review of the manuscript.

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    For example, some NMS appear to be caused or exacerbated by dopaminergic therapy and may therefore benefit from the reduced medication load associated with STN DBS. This can be especially helpful for psychosis, orthostatic hypotension (OH), daytime somnolence, or impulse control disorders (ICDs) (Ardouin et al., 2006; Bandini, Primavera, Pizzorno, & Cocito, 2007; Lim & Lang, 2010; Molina et al., 2000; Witjas et al., 2005; Witjas, Regis, Delphini, Peragut, & Azulay, 2007). In other cases reducing medications may lead to new-onset NMS, such as apathy, depression, or restless legs syndrome (RLS) (Kedia, Moro, Tagliati, Lang, & Kumar, 2004; Lhommée et al., 2012; Okun et al., 2005; Thobois et al., 2010).

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