Pathological Gambling in Parkinson's Disease

Pathological Gambling in Parkinson’s Disease

Mette Buhl Callesen, Jakob Linnet, Kristine Rømer Thomsen, Albert Gjedde, Arne Møller

PET Center, Aarhus University Hospital and Center of Functionally Integrative Neuroscience, Aarhus University.

 

The neurotransmitter dopamine is central to many aspects of human functioning, e.g., reward, learning, and addiction, including Pathological Gambling (PG), and its loss is key to Parkinson’s Disease (PD). PD is a neurodegenrative disorder caused by progressive loss of dopamine-producing cells in the midbrain [1]. One type of treatment of PD symptoms is medication that binds to dopamine receptors in the brain, i.e., dopamine agonists [1]. Unfortunately, for some PD patients a very serious side effect to this specific kind of treatment is developing PG. PG is an Impulse Control Disorder characterized by recurrent maladaptive behavior associated with personal, relational, and financial consequenses [2].

 

Since 2000, numerous reports have described PD patients who develop PG due to treatment with dopamine agonists [3-11]. The objective of the present project is to explain the pathogenesis of this particular complication to the treatment of PD patients. The aims are twofold, both driven by the main hypothesis that PD patients who develop PG secondary to treatment with dopamine agonists have a decreased sensitivity towards dopamine and hence an increased demand for dopamine. The neurophysiological subproject 1 uses PET imaging to determine changes of dopamine occupancy in the striatum in baseline and gambling situations. We will test the hypothesis that PD patients with PG secondary to dopamine agonism release more dopamine during gambling than PD patients without PG, pathological gamblers, and healthy controls. The behavioral subproject 2 uses a slot machine to test the hypothesis that PD patients with PG secondary to dopamine agonism have exacerbated gambling behavior compared to PD patients without PD, pathological gamblers, and healthy controls.  

 

References:

1.            Siegel, A. & Sapru, H.N. (2006). Lippincott, Williams & Wilkins. USA.

2.            DSM-IV-TR. (1994). Washington, DC: American Psychiatric Association. xxvii, 886.

3.            Seedat, S. et Al. (2000). Case Reports in Depression and Anxiety, vol. 11.

4.            Gschwandtner, U., et Al. (2001). Clinical Neuropharmacology, vol. 24 (3).

5.            Driver-Dunckley, E. et Al. (2003). Neurology, vol. 61.

6.            Avanzi, M. et Al. (2004). Neurol Sci.

7.            Dodd, M.L. et Al. (2005). Arch Neurol, vol. 62.

8.            Larner, A.J. (2006). Letters to the editors. Movement Disorders, vol. 21 (10).

9.            Grosset, K.A. et Al. (2006). Movement Disorders vol. 21(12).

10.            Avanzi, M. et Al. (2006). Movement Disorders vol. 21(12).

11.            Wong, S.H. et al. (2007). Letters to the editors, Movement Disorders, vol. 22 (4).