Characterization of chronic pain and somatosensory function in spinal cordinjury subjects

Citation
R. Defrin et al., Characterization of chronic pain and somatosensory function in spinal cordinjury subjects, PAIN, 89(2-3), 2001, pp. 253-263
Citations number
61
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
PAIN
ISSN journal
03043959 → ACNP
Volume
89
Issue
2-3
Year of publication
2001
Pages
253 - 263
Database
ISI
SICI code
0304-3959(200101)89:2-3<253:COCPAS>2.0.ZU;2-7
Abstract
The pathophysiology of the chronic pain following spinal cord injury (SCI) is unclear. In order to study it's underlying mechanism we characterized th e neurological profile of SCI subjects with (SCIP) and without (SCINP) chro nic pain. Characterization comprised of thermal threshold testing for warmt h, cold and heat pain and tactile sensibility testing of touch, graphesthes ia and identification of speed of movement of touch stimuli on the skin. In addition, spontaneously painful areas were mapped in SCIP and evoked patho logical pain - allodynia, hyperpathia and wind-up pain evaluated for both g roups. Both SCIP and SCINP showed similar reductions in both thermal and ta ctile sensations. In both groups thermal sensations were significantly more impaired than tactile sensations. Chronic pain was present only in skin ar eas below the lesion with impaired or absent temperature and heat-pain sens ibilities. Conversely. all the thermally impaired skin areas in SCIP were p ainful while painfree areas in the same subjects were normal. In contrast, chronic pain could be found in skin areas without any impairment in tactile sensibilities. Allodynia could only be elicited in SCIP and a significantl y higher incidence of pathologically evoked pain (i.e. hyperpathia and wind -up pain) was seen in the chronic pain areas compared to SCINP. We conclude that damage to the spinothalamic tract (STT) is a necessary condition for the occurrence of chronic pain following SCI. However, STT lesion is not a sufficient condition since it could also be found in SCINP. The abnormal ev oked pain seen in SCIP is probably due to neuronal hyperexcitability in the se subjects. The fact that apparently identical sensory impairments manifes t as chronic pain and hyperexcitability in one subject but not in another i mplies that either genetic predisposition or subtle differences in the natu re of spinal injury determine the emergence of chronic pain following SCI. (C) 2001 International Association for the Study of Pain. Published by Else vier Science B.V. All rights reserved.