[Pathological gambling and Parkinson disease].
[Pathological gambling and Parkinson disease].
Where did the research take place?
The study site has not been established. Author addresses may differ from where the research occurred.
Tochigi, JP · Author affiliation
Division of Neurology, Department of Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke-shi, Tochigi 329-0498, Japan.Location evidence
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Original abstract
Pathological gambling (PG) is defined by the DSM IV criteria as inappropriate, persistent, and maladaptive gambling behavior that has repercussions on family, personal, and professional life. It is classified as an impulse control disorder and is widely understood as a nonpharmacological addiction. PG has been reported as a complication in the treatment of Parkinson disease (PD). The prevalence of PG in PD has been reported to range between 1.7 and 7% compared to a prevalence of approximately 1% in the general population. Though there is no survey that indicates the prevalence of PG in Japanese PD patients, problematic gambling behaviors in PD are occasionally observed. In addition to PG other impulse control behaviors and punding (repetitive stereotyped behavior) are recognized as components of the dopamine dysregulation syndrome (DDS), which is characterized by the compulsive use of dopaminergic medications, including levodopa and subcutaneous apomorphine. Though PG can occur with DDS it often occurs in isolation. The vast majority of PG seen in PD is related to dopamine agonists (DA). With regard to the administration of oral DA, pramipexole may induce a higher degree of PG than other types of oral DA due to its disproportionate stimulation of dopamine D3 receptors. However, the differences between the observed effects of various classes of oral DA were insignificant. PG associated with levodopa mono-therapy is uncommon, but in the majority of cases levodopa is co-prescribed. Subthalamic nucleus deep brain stimulation (STN-DBS) was recently introduced to treat advanced PD. An improvement in PG symptoms following STN-DBS has been reported due to a marked decrease in dopaminergic medications. However, in some patients, PG developed following STN-DBS despite the significant reduction or discontinuation of DA. STN-DBS per se may be a potential initiator of PG. Younger age of PD onset, novelty seeking personality traits, history of alcohol abuse, and impulsivity traits were significant predictors of PG. Patients especially those with individual susceptibility to PG should be warned of the potential risks of PG before DA treatment is initiated.