Although Parkinson's disease selectively alters motor function, its victims frequently experience pain at some point during the course of their disease. Pain is rarely mentioned, however, in descriptions of the clinical aspects of Parkinson's disease, perhaps because the motor disorders are far more conspicuous or because the pain often occurs at a stage when the patient's ability to communicate discomfort is impaired. The mechanism of Parkinson's disease-associated pain remains obscure. About 50% of Parkinson's disease patients develop primary or secondary pain syndromes at some time during the course of their disease. The existence of primary pain syndromes suggests that the basal ganglia may contribute to nociception, a possibility that is consistent with current knowledge on neuron network connections, neurotransmitter effects, and interactions between dopaminergic, somatosensory, and endogenous opioid systems. Secondary pain syndromes include reflex sympathetic dystrophy syndrome, pain due to postural disorders, painful dystonia, and rheumatic or pseudorheumatic manifestations. The treatment of Parkinson's disease-associated pain remains poorly standardized. A better understanding of the pathophysiological mechanisms involved would probably lead to therapeutic improvements.