Send to

Choose Destination
See comment in PubMed Commons below
Eur J Nucl Med Mol Imaging. 2010 Aug;37(8):1512-20. doi: 10.1007/s00259-010-1436-y. Epub 2010 Mar 28.

Subthalamic nucleus stimulation affects limbic and associative circuits: a PET study.

Author information

Service de Médecine Nucléaire, Centre Eugène Marquis, rue de la Bataille Flandres Dunkerque, 35042 Rennes, France.



Although high-frequency deep brain stimulation of the subthalamic nucleus (STN DBS) improves motor symptoms in advanced Parkinson's disease (PD), clinical studies have reported cognitive, motivational and emotional changes. These results suggest that the STN forms part of a broadly distributed neural network encompassing the associative and limbic circuits. We sought to pinpoint the cortical and subcortical brain areas modulated by STN DBS, in order to assess the STN's functional role and explain neuropsychological modifications following STN DBS in PD.


We studied resting state glucose metabolism in 20 PD patients before and after STN DBS and 13 age-matched healthy controls using (18)F-FDG PET. We used statistical analysis (SPM2) first to compare pre-stimulation metabolism in PD patients with metabolism in healthy controls, then to study metabolic modifications in PD patients following STN DBS.


The first analysis revealed no pre-stimulation metabolic abnormalities in associative or limbic circuitry. After STN DBS, metabolic modifications were found in several regions known for their involvement in the limbic and associative circuits.


These metabolic results confirm the STN's central role in associative and limbic basal ganglia circuits. They will provide information for working hypotheses for future studies investigating neuropsychological changes and metabolic modifications related to STN DBS, with a view to improving our knowledge of this structure's functional role.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center