No abstract

Spinal cord injury (SCI) frequently results in neuropathic pain. However, the pathophysiology underlying this pain is unclear. In this study, we compared clinical examination, quantitative sensory testing (QST) and somatosensory evoked potentials (SEPs) in SCI patients with and without pain below spinal lesion level, with a control group of 20 subjects without injury. All patients had a traumatic SCI with a lesion above T10; 20 patients presented with spontaneous central neuropathic pain below lesion level, and 20 patients had no neuropathic pain or dysaesthesia. Patients with and without pain had a similar reduction of mechanical and thermal detection and pain thresholds, and SEPs. SCI patients with central pain more frequently had sensory hypersensitivity (brush- or cold-evoked pain, dysaesthesia or pinprick hyperalgesia) in dermatomes corresponding to lesion level than SCI patients without pain. There was no difference in intensity of pain evoked by repetitive pinprick at lesion level between patient groups. There was a significant correlation between intensity of brush-evoked dysaesthesia at lesion level and spontaneous pain below lesion level of SCI. These data suggest that lesion of the spinothalamic pathway alone cannot account for central pain in SCI patients, and that neuronal hyperexcitability at injury or higher level may be an important mechanism for pain below injury level.

Overall, our data do not support an immediate beneficial effect of PTH replacement therapy on muscle function or QoL. A high frequency of hypercalcemia among our patients may have compromised the potential beneficial effects of reversing the state of PTH insufficiency.

The findings support previous reports of sensory involvement in ALS, and raise the question of whether patients with ALS with sensory nerve abnormalities represent a variant of ALS. ALS associated with generalised sensory system abnormalities may be consistent with degeneration of motor neurones and dorsal root ganglion cells.