Bengt Skoog, Karl-Erik Jakobsson
Dep Rehabilitation Medicine, Institute of Clinical Neuroscience, Gothenburg, Sweden. E-mail: bengt.skoog@vgregion.se
DOI: 10.2340/20030711-1000039

Objective: To evaluate spasticity and below-level spinal cord injury neuropathic pain after spinal cord injury in patients with, or without, damage to the lumbar spinal cord and roots.
Design/patients: Chart review of 269 patients with spinal cord injury from segments C1 to T11.
Methods: Patients were interviewed concerning leg spasticity and below-level spinal cord injury neuropathic pain in the lower trunk and legs. Damage to the lumbar spinal cord and roots was inferred where there was radiological evidence of a vertebral fracture, spinal stenosis or the narrowing of spinal foramina of a vertebra from thoracic 11 to lumbar 5, or; magnetic resonance imaging showing evidence of damage to the lumbar spinal cord and roots.
Results: Among 161 patients without damage to the lumbar spinal cord and roots, 87% of those with cervical spinal cord injury experienced spasticity, compared with 85% with thoracic spinal cord injury. The corresponding figures for patients in whom damage to the lumbar spinal cord and roots was present were 57% and 52%, respectively. Below-level spinal cord injury neuropathic pain was not associated with damage to the lumbar spinal cord and roots. In those patients with no damage to the lumbar spinal cord and roots, regression showed that neither outcome was significantly associated with the level of spinal cord injury.
Conclusion: The lack of segmental dependency for spinal cord injury and spasticity suggests mechanisms restricted mainly to the lumbar spinal cord. For below-level spinal cord injury neuropathic pain, additional mechanisms, other than lesions of the spino-thalamic tract, must be considered.

Following a spinal cord injury, symptoms of increased nerve cell activity in the central nervous system appear, e.g. involuntary muscle activity (spasticity), below level neuropathic pain and urinary leakage. The distribution of overactive neurons is still unresolved. This chart review showed that leg spasticity was more frequent in patients with a cervical or thoracic spinal cord injury if the patients had no signs of damage to the lumbar spinal cord and roots. The occurrence of leg spasticity and below level spinal cord injury neuropathic pain was unrelated to each other or to the level of the spinal cord injury. This suggests that the mechanisms behind leg spasticity are mainly restricted to the lumbar spinal cord. For this pain, additional mechanisms other than lesions of the spino-thalamic tract must be considered