Parkinson disease (PD) is known to affect multiple neurotransmitter systems, resulting in both motor and nonmotor symptoms. Pain is an underrecognized but important nonmotor symptom of PD that may be very disabling and is known to impair quality of life.1 While significant progress has been made in ameliorating motor symptoms using pharmacological, rehabilitative, and surgical treatments, the treatment of pain in this context has not received sufficient attention. A literature review2 noted a reported prevalence of pain in PD of 40% to 85%, yet only about half of patients with PD who felt pain took analgesics. Classifying PD-related pain into its subtypes3 is important for rational treatment, and the most common subtypes of pain in PD are musculoskeletal and dystonic, with central neuropathic pain being the least common.2 To address pain successfully in PD, an understanding of its pathogenesis is important, yet this has remained elusive, in part because its causes are protean. Just as certain motor symptoms of PD are more responsive to dopaminergic drugs and deep brain stimulation (DBS), some pain subtypes may respond better than others to pharmacological and surgical intervention. Dysfunction of both dopaminergic and nondopaminergic basal ganglia pathways are likely to be involved in PD-related pain, which may explain why some types of pain are responsive to levodopa and others are not.4 Deep brain stimulation of the subthalamic nucleus (STN) is now an established treatment of disabling motor symptoms in advanced PD, and it is therefore important to understand its effect on pain associated with PD. Previous reports5,6 on the effects of STN DBS on pain in PD show that the levels of musculoskeletal and dystonic pain decreased when assessed 1 year after surgery, but, to our knowledge, there is no existing information on the status of chronic pain.