Converging preclinical, and human epidemiological, neuroimaging, and genetic evidence suggests a central role for dopamine neurotransmission in modulating pain perception and analgesia. Dysregulation in dopamine signaling may modulate the experience of pain both directly, by enhancing or diminishing the propagation of nociceptive signals, and indirectly, by influencing affective and cognitive processes, which affect the expectation, experience, and interpretation of nociceptive signals. Hypersensitivity to pain and high rates of comorbid chronic pain are common in disorders linked with deficits in dopamine system function, including disorders of mood and affect, substance abuse, and Parkinson disease. Hyposensitivity to pain, however, is common in patients with schizophrenia, which has been linked with excessive dopamine neurotransmission. Although patients are typically affected most by the primary symptoms of their disorders, alterations in pain perception may further increase the burden of their illness, compromising their quality of life. The present review focuses on this relationship, and discusses clinical and potential therapeutic implications for both patients with dopamine-related disorders and those with chronic pain syndromes.
aNational Institute of Mental Health, Bethesda, MD, USA
bDepartment of Medicine, Oppenheimer Family Center for Neurobiology of Stress, University of California, Los Angeles, CA, USA
cDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, CA, USA
dBrain Research Institute, University of California, Los Angeles, CA, USA
*Corresponding author. Address: Gail and Gerald Oppenheimer Family, Center for Neurobiology of Stress, University of California, CHS 42-210, 10833 Le Conte Avenue, Los Angeles, CA 90095-7378, USA. Tel.: +1 310 206 0192.
Submitted June 28, 2011; revised November 29, 2011; accepted January 4, 2012.