Positron emission tomography in Parkinson’s disease: insights into impulsivity

Abstract

This study reviews previous studies that employ positron emission tomography (PET) imaging assessments in Parkinson’s disease (PD) patients with and without Impulsive Compulsive Behaviours (ICB). This begins with a summary of the potential benefits and limitations of commonly utilized ligands, specifically D_2/3 receptor and dopamine transporter ligands. Since previous findings emphasize the role of the ventral striatum in the manifestation of ICBs, this study attempts to relate these imaging findings to changes in behaviour, especially emphasizing work performed in substance abuse and addiction. Next, it reviews how increasing disease duration in PD can influence dopamine receptor expression, with an emphasis on differential striatal and extra-striatal changes that occur along the course of PD. Finally, it focuses on how extra-striatal changes, particularly in the orbitofrontal cortex, amygdala, and anterior cingulate, may influence the proficiency of behavioural regulation in PD. The discussion emphasizes the interaction of disease and medication effects on network-wide changes that occur in PD, and how these changes may result in behavioural dysregulation.

Keywords:

• Parkinson’s disease
• impulse control
• dopamine receptors
• PET imaging
• ventral striatum

Disclosure statement

D.C. has received personal fees from AbbVie, Acadia, Huntington Study Group, Lundbeck, Neurocrine, Teva Neuroscience, outside of submitted work. A.S. has no conflicts of interest.

Additional information

Funding

D.C. has received grant support from the National Institutes of Health [NINDS; R01NS097783, K23NS080988], Michael J. Fox Foundation, as well as AbbVie, Bristol-Myers Squibb, C2N, CHDI, Eli Lilly, Teva, Vaccinex, and Wave Pharmaceuticals.