Neurophysiologic study of central pain in patients with Parkinson disease

Patients with Parkinson disease (PD) may present with various types of pain. In some instances, no cause can be identified and pain is considered a primary disorder (primary central pain [PCP]). We hypothesized that PCP in patients with PD (PD-PCP) may be due to a dysfunction of pain pathways or the processing of pain inputs in the CNS.

We carried out a psychophysical and neurophysiologic study in 9 patients with PD-PCP, 9 patients with PD without pain (PD-NoP), and 9 healthy control subjects. We assessed the clinical characteristics of pain, performed quantitative sensory testing with thermal probes, and recorded laser-evoked potentials (LEPs) and laser-induced sudomotor skin responses (1-SSRs) in "off" and "on" conditions.

In "off" condition, patients with PD-PCP had lower heat pain and laser pinprick thresholds, higher LEP amplitudes, and less habituation of the l-SSR in comparison with PD-NoP patients and control subjects. Abnormalities were more marked in the most affected side. In "on" condition, psychophysical and neurophysiologic differences disappeared or were significantly attenuated.

Conduction along peripheral and central pain pathways is normal in patients with Parkinson disease with or without primary central pain. However, apart from signs of hyperalgesia, our patients exhibited lack of habituation of sympathetic sudomotor responses to repetitive pain stimuli, suggesting an abnormal control of the effects of pain inputs on autonomic centers. Abnormalities were attenuated by l-dopa, suggesting that the dysfunction may occur in dopamine-dependent centers regulating both autonomic function and inhibitory modulation of pain inputs.