Pain sensitivity in Parkinson’s
disease (PD) is known to be altered in a L-dopa-dependant
manner with increased spinal nociception and experimental
pain perception in the medication-defined “off” state. As
Parkinson’s disease-related pain can be an early symptom,
this study aimed to detect how far experimental pain
sensivity and spinal nociception are changing in the course
of the disease. For this purpose, 29 PD patients and 27
healthy control persons were tested in regard to their heat
and electrical pain thresholds. In addition, the nociception
flexion reflex (NFR) threshold was assessed as a marker of
spinal nociception. To exclude confounding factors (e.g.
depression, dementia, anxiety and pain of other origin), all
participants completed a selection of questionnaires whose
requirements had to be fulfilled to participate in the study.
The severity of disease was classified by using the
well-established Unified Parkinson Disease Rating Scale
(UPDRS) motor score under their usual medication (“on”
state). Based on this score, the patients were divided into
three severity groups for further analysis. The
electrophysiological investigation of the pain and NFR
thresholds took place in the morning between 6 and 9 a.m. in
the medication-defined “off” state. Data provided evidence
for a preserved spinal nociception and pain sensitivity in
the early state of Parkinson’s disease. Following increased
spinal nociception, also electrical and heat pain thresholds
decreased in the course of disease. These findings support
the assumption that PD-related pain might arise because of
modified spinal nociception, which increases in the course of
the disease. Regarding current studies, central and
peripheric mechanisms are also considered to influence pain
perception. The central dopaminergic and noradrenergic system
as well as the descending inhibitory control system likely
affect pain processing in PD. Also cutaneous denervation is
supposed to be responsible for the sensory deficit of PD
patients.