Neuropathic Pain in Parkinson's Disease.

Pain is a well-recognized and important non-motor manifestation in Parkinson disease (PD). Painful or unpleasant sensations in PD can be classified as musculoskeletal, dystonia, akathisia, radicular, and central or primary pain; the last two are associated with neuropathic pain. Particularly, neuropathic pain in PD has not been fully clarified; therefore, it goes somewhat unnoticed, and the affected patients do not receive adequate pain treatment. The main purpose of this literature review was to identify the incidence of neuropathic pain in PD and the involvement of dopamine of this type of pain by the integration of different lines of investigation. In this review, a search was conducted using PubMed, ProQuest, EBSCO, Medline, EMBASE, and the Science Citation index for studies evaluating pain in patients with PD. The inclusion criteria were as follows: original articles that evaluated incidence and possible mechanism of neuropathic, central, and radicular pain in PD. Nine studies related to the incidence of neuropathic pain in PD suggest the activation of cerebral areas, such as the cortex, striatum, amygdala, thalamus, raphe nuclei, and locus coeruleus. Neuropathic pain is related to altered levels of dopamine, serotonin, and norepinephrine; these neurotransmitters are related to the sensitive and emotional dimensions of pain. Dopamine could cause hypersensitivity to pain, either indirectly through modulatory effects on affective pain processing and/or directly by affecting the neural activity in key areas of the brain that modulate pain. A considerable proportion of patients with PD suffer neuropathic pain; however, it has been disregarded, this has led to an inability to achieve an adequate treatment and a decrease in pain to improve the quality of life of these patients. We consider that neuropathic pain in PD is possibly induced by neurophysiological changes due to the degradation of dopaminergic neurons.

Chemical Mediators' Expression Associated with the Modulation of Pain in Rheumatoid Arthritis.

BACKGROUND: The management of pain in patients with rheumatoid arthritis (RA) is a complex subject due to the autoimmune nature of the pathology. Studies have shown that chemical mediators play a fundamental role in the determination, susceptibility and modulation of pain at different levels of the central and peripheral nervous system, resulting in interesting novel molecular targets to mitigate pain in patients with RA. However, due to the complexity of pain physiology in RA cand the many chemical mediators, the results of several studies are controversial. OBJECTIVE: The aim of this study was to identify the chemical mediators that are able to modulate pain in RA. METHOD: In this review, a search was conducted on PubMed, ProQuest, EBSCO, and the Science Citation index for studies that evaluated the expression of chemical mediators on the modulation of pain in RA. RESULTS: Few studies have highlighted the importance of the expression of some chemical mediators that modulate pain in patients with rheumatoid arthritis. The expression of TRPV1, ASIC-3, and TDV8 encode ionic channels in RA and modulates pain, likewise, the transcription factors in RA, such as TNFα, TGF-ß1, IL-6, IL-10, IFN-γ, IL-1b, mTOR, p21, caspase 3, EDNRB, CGRPCALCB, CGRP-CALCA, and TAC1 are also directly involved in pain perception. CONCLUSION: The expression of all chemical mediators is directly related to RA and the modulation of pain by a complex intra and extracellular signaling pathway, however, transcription factors are involved in modulating acute pain, while the ionic channels are involved in chronic pain in RA.