Somatosensory findings in patients with spinal cord injury and central dysaesthesia pain.

Abstract

Objective-To determine whether central pain in patients with spinal cord injury is only dependent on the lesioning of spinothalamic pathways. Methods-In sixteen patients with spinal cord injury and central dysaesthesia pain, somatosensory abnormalities in painful denervated skin areas were compared with somatosensory findings in normal skin areas as well as in non-painful denervated skin areas. Results-The threshold values for detection of thermal (heat, cold, heat pain, or cold pain) and tactile stimulation were significantly changed in denervated skin areas although there were no significant differences in the threshold values between painful and non-painful denervated skin areas. The reductions of sensations of touch, vibration, joint position, and two point discrimination in painful and non-painful denervated skin areas were not significantly different. Allodynia (pain caused by non-noxious stimulation) and wind up-like pain (pain caused by repeatedly pricking the skin) were significantly more common in painful than nonpainful denervated skin areas. Conclusions-Because pain and thermal sensory perception are primarily mediated to the brain via spinothalamic pathways, whereas the sensations of touch, vibration and joint position are primarily mediated by dorsal column-medial lemniscal pathways, the results indicate that central pain is not only dependent on the lesioning of either dorsal column-medial lemniscal pathways or spinothalamic pathways. The findings of abnormal evoked pain (allodynia and wind up-like pain) may be consistent with the experimental findings of hyperexcitability in nociceptive spinothalamic tract neurons, that may be involved in the pathogenesis of central pain. Severe and disabling chronic pain is a major sequel after spinal cord injury, with an estimated prevalence ranging from 18 to 63%.1 Pain in patients with spinal cord injury includes musculoskeletal pain, radicular pain, visceral pain, central dysaesthesia pain, psychogenic pain, lesional pain, reflex sympathetic dystrophy, and limb pain secondary to compressive mononeuropathies.2 Central dysaesthesia pain is characterised by spontaneous continuous and intermittent pain as well as by pain evoked by non-noxious stimulation (allodynia).2 It is difficult to treat this type of pain as central pain is not effectively relieved by traditional analgesics or neurosurgical procedures.34 Increased knowledge of the pathogenesis of central dysaesthesia pain after spinal cord injury is desired.An important hypothesis is that the development of central pain is dependent on the lesioning of spinothalamocortical pathways.35 The hypothesis is partly based on the finding that sensory perception mediated to the brain via spinothalamocortical pathways is more often affected than sensory perception mediated by dorsal column-medial lemniscal pathways in this group of patients.3 6In the present study, somatosensory testing of patients with spinal cord injury and central dysaesthesia pain was undertaken to further examine whether central pain is ...

Types and effectiveness of treatments used by people with chronic pain associated with spinal cord injuries: influence of pain and psychosocial characteristics

“…39,40 Allodynia Allodynia (ie, pain in response to a stimulus that would normally not provoke pain, such as light touch) or hyperalgesia (ie, an exaggerated response to a painful stimulus) is often associated with neuropathic pain. 18 Participants were asked to report whether any areas on their body only hurt or hurt more when the particular area was exposed to something that would normally not be painful, such as a breeze or light touch. These responses were used as surrogate measures indicating the presence of allodynia.…”

“…16,17 Several studies suggest that abnormal sensations may indicate specific mechanisms important for treatment decisions. [18][19][20][21] Sensory changes may be quantitative (threshold changes such as hypoesthesia or hyperesthesia) or qualitative (such as allodynia, dysesthesia, or paresthesia). 22,23 Responses to sensory testing may be important for defining a specific type of pain and thus serve as a basis for prescribing pain treatment.…”

Thermal perception thresholds: assessing the level of human spinal cord injury

“…Misinterpretation of thermal sensation and thermal allodynia were found in the present study in the ZPP of subjects with complete lesions and below the level in subjects with incomplete lesions but not above the level of lesion in either group. Thermal allodynia may have an explanation similar to that proposed for mechanical allodynia 31 whereby hyperexcitable dorsal horn neurones normally responding to noxious stimulation begin responding also to activity in low threshold mechanoreceptors. However, mechanical allodynia was not observed in any SCI subjects either above or below their injury.…”

Pathophysiological mechanisms of central neuropathic pain after spinal cord injury

“…In 16 patients with central neuropathic pain after traumatic SCI, we compared sensory loss in painful denervated skin areas with sensory loss in non-painful denervated skin areas. 23 An important observation was that sensory modalities mediated by spinothalamic pathways were not more signi®cantly impaired than sensory modalities mediated by dorsal column ± medial lemniscal pathways in the painful denervated skin areas compared to the non-painful denervated skin areas (Figure 1). Thus, in these patients dea erentation of spinothalamic pathways was not a su cient condition for development of central neuropathic pain.…”

“…Our data provided evidence that sensory loss must be coupled with abnormal pain responsiveness. 23 Abnormal pain perception Abnormal pain perception in the a ected regions of these patients include three di erent components: Spontaneous continuous pain (usually burning and aching in quality), spontaneous intermittent pain (usually stinging in quality) and abnormally evoked pain (usually produced by touch or movement). Stimulus-evoked pain may be abnormal leading to allodynia, hyperalgesia or hyperpathia.…”