Neuronal hyperexcitability is a key finding in patients with neuropathic pain. Contributing to hyperexcitability may be decreased activity in the endogenous pain inhibitory systems. The present study aimed at recruiting descending inhibition, by the use of painful heterotopic stimulation (HTS), in 16 patients with peripheral chronic neuropathic pain and associated brush-evoked allodynia. Two experiments were performed: one examined the effect of HTS on ongoing pain and intensity of brush-evoked allodynia and the other tested the effect of HTS on ongoing pain and area of brush-evoked allodynia. Both experiments consisted of two sessions, one with painful cold HTS (1 degrees C water bath) another with non-painful neutral HTS (32 degrees C water bath). The area of brush-evoked allodynia was significantly reduced (P=0.003) during painful HTS, as compared to non-painful HTS. In contrast, neither the intensity of brush-evoked allodynia nor the ongoing pain was significantly changed. The results indicate that endogenous pain modulating systems can alter some aspects of chronic neuropathic brush-evoked allodynia. The differential effect of painful HTS on ongoing pain and area of brush-evoked allodynia suggest that separate mechanisms are involved.
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http://dx.doi.org/10.1016/s0304-3959(02)00421-9 | DOI Listing |
Brain
September 2024
Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DU, UK.
Neuronal hyperexcitability is a key driver of persistent pain states including neuropathic pain. Leucine-rich, glioma inactivated 1 (LGI1), is a secreted protein known to regulate excitability within the nervous system and is the target of autoantibodies from neuropathic pain patients. Therapies that block or reduce antibody levels are effective at relieving pain in these patients, suggesting that LGI1 has an important role in clinical pain.
View Article and Find Full Text PDFPain
February 2021
Department of Anesthesiology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Mechanical allodynia is a debilitating condition for millions of patients with chronic pain. Mechanical allodynia can manifest in distinct forms, including brush-evoked dynamic and filament-evoked static allodynia. In the nervous system, the forkhead protein Foxo1 plays a critical role in neuronal structures and functions.
View Article and Find Full Text PDFJ Neurotrauma
June 2019
Department of Physiology, Emory University School of Medicine, Atlanta, Georgia.
Respiratory complications frequently accompany spinal cord injury (SCI) and slowed breathing has been shown to mitigate pain sensitivity. It is possible that elevated respiratory rates (RRs) signal the emergence of chronic pain after SCI. We previously validated the use of remote electric field sensors to noninvasively track breathing in freely behaving rodents.
View Article and Find Full Text PDFNeurosci Bull
April 2019
Department of Neurology, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200032, China.
Neuropathic pain is a chronic debilitating symptom characterized by spontaneous pain and mechanical allodynia. It occurs in distinct forms, including brush-evoked dynamic and filament-evoked punctate mechanical allodynia. Potassium channel 2.
View Article and Find Full Text PDFScand J Pain
April 2011
Clinical Pain Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Solna, SE-171 76 Stockholm, Sweden.
Introduction In order to develop valid experimental human pain models, i.e., models potentially reflecting mechanisms underlying certain expressions of clinical pain conditions, similarities and discrepancies of symptoms/signs must first and foremost be evaluated comparing the two.
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