Brain Advance Access originally published online on July 31, 2008
Brain 2008 131(9):2387-2400; doi:10.1093/brain/awn169
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Residual spinothalamic tract pathways predict development of central pain after spinal cord injury
1Prince of Wales Medical Research Institute, 2University of New South Wales, Australia, 3Department of Neurology, Division of Neurological Pain Research and Therapy, University-Clinic of Schleswig-Holstein, Campus Kiel, Germany and 4Prince of Wales Hospital, Randwick, Sydney, NSW, Australia
Correspondence to: Priv.-Doz. Dr Med. Gunnar Wasner, Department of Neurology, Division of Neurological Pain Research and Therapy, University Hospital of Schleswig-Holstein, Campus Kiel, Schittenhelmstrasse 10, 24105 Kiel, Germany E-mail: g.wasner{at}neurologie.uni-kiel.de
Central neuropathic pain following lesions within the CNS, such as spinal cord injury, is one of the most excruciating types of chronic pain and one of the most difficult to treat. The role of spinothalamic pathways in this type of pain is not clear. Previous studies suggested that spinothalamic tract lesions are necessary but not sufficient for development of central pain, since deficits of spinothalamic function were equally severe in spinal cord injured people with and without pain. The aim of the present study was to examine spinothalamic tract function by quantitative sensory testing before and after activation and sensitization of small diameter afferents by applying menthol, histamine or capsaicin to the distal skin areas where spontaneous pain was localized. Investigations were performed in matched groups each of 12 patients with and without central pain below the level of a clinically complete spinal cord injury, and in 12 able-bodied controls. To test peripheral C fibre function, axon reflex vasodilations induced by histamine and capsaicin applications were quantified. In eight patients with pain, sensations of the same quality as one of their major individual pain sensations were rekindled by heat stimuli in combination with topical capsaicin (n = 7) or by cold stimuli (n = 1). No sensations were evoked in pain-free patients (P < 0.01). Capsaicin-induced axon reflex vasodilations were significantly larger in pain patients with heat- and capsaicin-evoked sensations in comparison to pain patients without capsaicin-provoked sensations. These results suggest that intact thermosensitive nociceptive afferents within lesioned spinothalamic tract pathways distinguish people with central pain from those without. The ability to mimic chronic pain sensations by activation of thermosensory nociceptive neurons implies that ongoing activity in these residual spinothalamic pathways plays a crucial role in maintaining central pain. We propose that processes associated with degeneration of neighbouring axons within the tract, such as inflammation, may trigger spontaneous activity in residual intact neurons that act as a ‘central pain generator’ after spinal cord injury.
Key Words: spinal cord injury; central neuropathic pain; spinothalamic tract; sensitization; nociceptive afferents
Abbreviations: NRS, numeric rating scales; SCI, spinal cord injury; ZPP, zone of partial preservation
Received April 25, 2008. Revised June 19, 2008. Accepted July 2, 2008.