M Buonocore1, C Bonezzi. 1. Unit of Clinical Neurophysiology, Salvatore Maugeri Foundation IRCCS, Scientific Institute of Pavia, Pavia, Italy. mbuonocore@fsm.it
Abstract
AIM: Pain resulting from nerve lesions is classically referred to as a ''burning pain''. Both the axonal damage and sensitization of unmyelinated C-fibres have been considered as the possible generators of this sensation. The aim of this study was to verify the hypothesis that hot-burning sensations are produced by the axonal damage of afferent unmyelinated fibres in peripheral nerves. METHODS: A total of 122 patients with pain localised in the distal parts of the upper limbs (hand, forearm) and lower limbs (leg or foot) were enrolled in the study. The intensity of pain and hot-burning sensations was measured using a numerical scale (range 0-10). The relationship between the presence of warm hypoesthesia (related to the loss of afferent unmyelinated fibres) and hot-burning sensations was assessed. Warm hypoesthesia was identified by Quantitative Sensory Testing employing thermal stimulation (QST-t) and the patients were divided into 2 groups: group A, with hypoesthesia and group B with normoesthesia. Patients with a central nervous impairment were excluded. RESULTS: No significant differences in the intensity of pain and hot-burning sensations was observed between the group of patients with warm hypoesthesia and that with warm normoesthesia. CONCLUSIONS: This study does not confirm the hypothesis that hot-burning sensations are produced by the axonal damage of afferent amyelinated fibres in peripheral nerves. It agrees with clinical evidence suggesting that patients with different clinical conditions can complain of hot-burning sensations, independently of the presence of a nerve lesion.
AIM: Pain resulting from nerve lesions is classically referred to as a ''burning pain''. Both the axonal damage and sensitization of unmyelinated C-fibres have been considered as the possible generators of this sensation. The aim of this study was to verify the hypothesis that hot-burning sensations are produced by the axonal damage of afferent unmyelinated fibres in peripheral nerves. METHODS: A total of 122 patients with pain localised in the distal parts of the upper limbs (hand, forearm) and lower limbs (leg or foot) were enrolled in the study. The intensity of pain and hot-burning sensations was measured using a numerical scale (range 0-10). The relationship between the presence of warm hypoesthesia (related to the loss of afferent unmyelinated fibres) and hot-burning sensations was assessed. Warm hypoesthesia was identified by Quantitative Sensory Testing employing thermal stimulation (QST-t) and the patients were divided into 2 groups: group A, with hypoesthesia and group B with normoesthesia. Patients with a central nervous impairment were excluded. RESULTS: No significant differences in the intensity of pain and hot-burning sensations was observed between the group of patients with warm hypoesthesia and that with warm normoesthesia. CONCLUSIONS: This study does not confirm the hypothesis that hot-burning sensations are produced by the axonal damage of afferent amyelinated fibres in peripheral nerves. It agrees with clinical evidence suggesting that patients with different clinical conditions can complain of hot-burning sensations, independently of the presence of a nerve lesion.