Parkinson’s Medicines May Contribute to Somatosensory Deficits, Study Finds

Antiparkinsonian medicines may cause Parkinson’s patients to develop abnormal sensitivity to temperature, touch and pain, according to a recent study.

The study, “Quantitative Sensory Testing (QST) in Drug-Naïve Patients with Parkinson’s Disease” was published in the Journal of Parkinson’s Disease.

The somatosensory system is composed of neurons that make the conscious perception of touch, pressure, pain, temperature, position, movement, and vibration possible.

Evidence supports that Parkinson’s patients have somatosensory deficits, including perception of temperature, touch and one’s body position in space. Moreover, and although there is still no clear physiological explanation for it, most Parkinson’s patients experience pain before motor symptoms’ onset.

However, most studies on this matter have been performed on medicated patients and have generated inconsistent results, which seems to imply that dopaminergic medication — the gold-standard Parkinson’s treatment — may influence patients’ somatosensory abilities.

To assess whether dopaminergic medication contributes to sensory processing abnormalities, researchers from the University Medical Center Hamburg-Eppendorf and the University Hospital Essen in Germany set up to investigate sensitivity to temperature, touch, and pain in Parkinson’s patients who had never taken antiparkinsonian drugs.

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To do so, they used the well-established quantitative sensory testing (QST) protocol. Quantitative sensory testing determines the sensation and pain thresholds for cold and warm temperatures, and the vibration sensation threshold by stimulating the skin and comparing the results to normative values.

Researchers assessed 13 somatosensory parameters including cold and warm detection thresholds, perception of changing temperatures from warm to cold and vice versa, perception of cold as heat, cold and heat pain thresholds, mechanical detection and mechanical pain thresholds, sensitivity to pinprick stimuli, pressure pain threshold, vibration detection thresholds, experience of pain during innocuous dynamic tactile stimulation and temporal summation of pain (i.e. increased perception of pain to repetitive painful stimuli).

Nineteen dopaminergic, drug-naïve Parkinson’s patients (ages 42–82) and 19 age, sex and dominant hand-matched healthy subjects were examined.

Compared to the control group, somatosensory processing of drug-naïve patients was normal. However, previous research showed medicated Parkinson’s patients have increased sensitivity to temperature and pain plus reduced sensitivity to touch. Therefore, considering the results of non-medicated subjects, researchers assume the possibility of a role for dopaminergic medication in somatosensory disability.

Investigators also tested differences between the more affected body side and the less affected one, but no significant changes were observed. In addition, no relevant alteration was found in somatosensory characteristics of patients with or without disease-specific chronic pain and with distinct disease subtypes (tremor-dominant, akinetic-rigid or mixed).

However, age, but not disease severity, was negatively associated with warm and mechanical detection thresholds, suggesting a decrease in patients’ ability to sense temperature and touch with increasing age. Although less pronounced, these findings were also observed in elderly controls.

Of note, this study’s small sample size with an average disease duration of almost two years (a range of 6–67 months) could constitute a selection bias toward patients with less severe disease (because disease severity progresses with age/disease duration), which could in turn influence the analysis.

“[S]omatosensory abnormalities previously reported in medicated [Parkinson’s disease] patients might rather be a result of dopaminergic medication or may occur later in the course of the disease or with increasing age,” researchers said.