Abstract

The chronic neuropathic pain of spinal cord injury origin has been shown to be related to permanent neurochemical changes in the dorsal horn neurons thus producing spontaneous discharges of central nociceptive neurons resulting in chronic pain. There is a doubt, however, regarding the possible supraspinal neurogenic mechanism contributing to the generation of this chronic neuropathic pain phenomenon.To address this issue we determinated the functional condition of the thalamocortical transsmission by obtaining somatosensory evoked potentials from the stimulation of median nerves in the group of 23 paraplegics suffering from chronic posttraumatic neuropathic pain. We prospectively collected and analysed data from 23 patients, 21 males and 2 females, aged from 22 to 59 years (mean age, 35.8 y) suffered from chronic neuropathic pain of the spinal cord and cauda equina injury origin who underwent neurophysiological investigation by obtaining somatosensory evoked potentials from the stimulation of median nerves. Somatosensory evoked potentials were defined according to three-grade scale: normal findings (C), slightly abnormal (B), abnormal findings (A). Our findings revealed pathological somatosensory evoked potentials in 17 patients (73.9%). Only 3 (13%) patients had normal findings, and 3 (13%) slightly abnormal according to our criteria. Pathological findings in a majority of our patients, with changes in the primary cortical complex N20-P25, could be indicative for the dysfunction of thalamocortical afferences in patients with paraplegic pain.

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