What Is In A Name?

We read with interest the OXYDOPA study by Brefel-Courbon et al,¹ where central pain in people with Parkinson's disease (PwP) was treated by prolonged-release oxycodone, increase in levodopa, or placebo. The authors should be complimented for conducting such a complex multicenter trial on a topic that needs urgent new data and that extended itself through times of coronavirus disease pandemics. Bravo.

Pain is among the most burdensome non-motor symptoms of Parkinson's disease (PD) and to date no effective evidence-based treatment exists for its control. Different pain types have different mechanisms of disease, which respond differently to therapeutic interventions. This means that clinicians should first assess the pain type PwP have and then proceed to a specific therapy.

To do that, three steps need to be completed. First, clinicians need to ascertain that pain is chronic (ie, being present most of the days for more than 3 months). Interestingly, several classification systems for pain in PD do not ascertain that pain is chronic. Second, since pain affects at least 20% of the general population, one needs to ascertain that chronic pain in PwP is related to PD. By ignoring this point, one risks misclassifying, for example, migraine, or previously existing fibromyalgia as PD-related pain. More than 20% of PwP have pains not related to the disease. Third, the classification should acknowledge general classification frameworks and previous knowledge generated by the field of PD and pain.²

The present study aimed at chronic pain in PwP, therefore, fulfilling the first step. However, it classified PD-related pain using a classification system that has not yet been validated. There was no reference to the relationship between patient's pain and PD. Therefore, the study sample may have included PwP with different pain mechanisms.

What is more problematic is the use of “central neuropathic pain.” Central neuropathic pain because of PD does not stand with any current classification of central neuropathic pain (see Table 1).³ There is no doubt that the clinical phenotype described as being of central neuropathic pain exists in PwP, but it is rare.⁴

The authors also mixed the concept of “central neuropathic pain” with “central parkinsonian pain.” The problematic definition of the pain type under study makes the results of this study difficult to apply to the clinical practice.

“Central parkinsonian pain” fits the definition of nociplastic pain (as suggested in the very same paper used for pain classification in the present study)⁵ (Table 1). The classification of PD-related pains according to its mechanistic descriptors (nociceptive, neuropathic, and nociplastic) has been validated clinically, has shown to provide different profiles of somatosensory and cortical excitability changes in PwP,⁶ and recently shown to be useful when performing neuromodulation strategies for pain relief in PwP.⁷ The study of pain is an area of rich intersection between fields and the use of proper nomenclature and validated classification frameworks will only make the field of pain in PD move faster, for the sake of patients.

Nothing to report.

1. Research project: A. Conception, B. Organization, C. Execution; 2. Manuscript preparation: A. Writing of the first draft, B. Review and critique.

D.C.A.: 1B, 2A, 2B

V.M.: 1B, 2A, 2B

S.P.L.: 1B, 2A, 2B