According to Defazio et al,1 4.5% of patients with Parkinson disease (PD) have central pain (CP) as compared with 1.6% of control subjects. The association was reportedly significant.
Whereas the International Association for the Study of Pain defines CP as pain initiated or caused by a primary lesion or dysfunction of the central nervous system, this definition is known to be too extensive. A better definition is spontaneous, constant, and/or evoked pain, dysesthesia, or pruritus initiated by a central nervous system lesion impinging on or interfering with the spinothalamoparietal (STP) pathway.2 As such, PD is not associated with CP as the function of the STP pathway is normal from receptor to cortex.3 Rather, CP-like pain should be renamed CP-allied condition (CPAC)2 to mark this difference. The generator of CP is an unbalanced thalamoparietal oscillatory axis,2 whereas PD CPAC is most likely due to disrupted inhibition of the somatosensory system from the striopallidal system (see the full discussion by Canavero and Bonicalzi2).
Canavero S. Central Pain and Parkinson Disease. Arch Neurol. 2009;66(2):282–283. doi:10.1001/archneurol.2008.545
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