Characterization of chronic pain and somatosensory function in spinal cord injury subjects

Abstract

The pathophysiology of the chronic pain following spinal cord injury (SCI) is unclear. In order to study it's underlying mechanism we characterized the neurological profile of SCI subjects with (SCIP) and without (SCINP) chronic pain. Characterization comprised of thermal threshold testing for warmth, cold and heat pain and tactile sensibility testing of touch, graphesthesia and identification of speed of movement of touch stimuli on the skin. In addition, spontaneously painful areas were mapped in SCIP and evoked pathological pain--allodynia, hyperpathia and wind-up pain evaluated for both groups. Both SCIP and SCINP showed similar reductions in both thermal and tactile sensations. In both groups thermal sensations were significantly more impaired than tactile sensations. Chronic pain was present only in skin areas below the lesion with impaired or absent temperature and heat-pain sensibilities. Conversely, all the thermally impaired skin areas in SCIP were painful 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 significantly 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 evoked pain seen in SCIP is probably due to neuronal hyperexcitability in these subjects. The fact that apparently identical sensory impairments manifest as chronic pain and hyperexcitability in one subject but not in another implies that either genetic predisposition or subtle differences in the nature of spinal injury determine the emergence of chronic pain following SCI.

International Spinal Cord Injury Pain Classification: part I. Background and description

“…Neuropathic pain that occurs in this distribution and that cannot be attributed to the spinal cord damage should be classified as other (neuropathic) pain. The presence of below-level SCI pain is suggested by characteristics such as: 4,5,9,16,[20][21][22] Sensory deficits within the pain distribution Allodynia or hyperalgesia within the pain distribution (for persons with incomplete injury) Endorsement of one or more of the following pain descriptors: 'hot-burning' , 'tingling' , 'pricking' , 'pins and needles' , 'sharp' , 'shooting' , 'squeezing' , 'painful cold' and 'electric shock-like' Below-level SCI pain can occur in persons with complete injuries and in those with incomplete injuries. Neuropathic pain associated with cauda equina damage is radicular in nature, and therefore defined as at-level SCI (neuropathic) pain, regardless of distribution.…”

Pain following spinal cord injury

“…(4) Abnormal sensations, ie, allodynia, hyperpathia and increased windup pain could only be evoked in painful regions. 6 Thus, our ®ndings show that damage to the anterolateral spinothalamic system, and not the dorsal column, is indeed a necessary but not a su cient condition for the development of chronic pain.…”

“…Consistent with Beric et al we found a signi®cant impairment of spinothalamic function with relative preservation of dorsal column function in incomplete SCI subjects with chronic pain below the lesion. 6 Temperature and pain perception was much more impaired than touch, graphesthesia and identi®cation of speed of movement in body areas below the lesion. However, our control group of SCI subjects who did not su er from chronic pain exhibited an almost identical imbalance between spinothalamic and dorsal column function.…”

“…Furthermore, in chronic pain patients, we could not establish any relationship between the degree of this imbalance and the intensity of chronic pain. 6 Thus, the suggestion of Beric et al that chronic dysesthetic syndrome develops due to loss of spinothalamic system with limited damage to dorsal column function is not an adequate explanation for the appearance of this syndrome.…”

“…In contrast, those SCI patients who do not su er from chronic pain show spinothalamic damage, which is almost identical in magnitude to chronic pain patients but in no case shows evidence of neuropathic pain. 6 The idea that there is a genetic predisposition for the emergence of chronic pain has already been proposed to account for the fact that chronic pain does not always occur after peripheral nerve injury. 7 ± 9 We believe that such an explanation is also tenable when damage of central nociceptive neurons occurs.…”