Original ReportNeuropathic Pain and Functional Reorganization in the Primary Sensorimotor Cortex After Spinal Cord Injury

- Limited large-scale cortical reorganization was observed after human spinal cord injury.
- Neuropathic pain was not associated with increased plasticity in the brain.
- Reorganization in the central nervous system could be an adaptive process preventing development of neuropathic pain.

Refractory to most types of treatment, neuropathic pain (NP) is a major problem for people living with spinal cord injury (SCI). The underlying mechanisms among problems related to treatment are poorly understood. The aim of the present study was to investigate the association between cortical reorganization and NP after SCI. Twenty-four individuals with sensorimotor complete and incomplete paraplegia and tetraplegia (12 with NP, 13 pain free) and 31 healthy individuals were examined. Functional magnetic resonance imaging was used to assess activation in primary somatosensory and motor cortices in response to motor (ie, active and passive wrist extension) and sensory (ie, heat and brushing) tasks applied on the dorsum of the hand. In individuals with SCI, there were no group-level differences in task-related activation (ie, movement or sensory) compared with the healthy controls. However, based on the Euclidean distance measure, individuals with SCI demonstrated a lateral shift of peak activity in primary sensory and motor cortices (P < .05). Among those with NP, chronic pain intensity inversely correlated with the magnitude of the shift in the primary motor cortex during active wrist extension. The findings reveal that NP in motor and sensory tasks at or above the level of the lesion is not associated with increased plasticity. In line with previous studies, changes in somatotopy and activation after SCI are rather limited and the influence of NP on plasticity remains controversial.PerspectiveUsing functional magnetic resonance imaging, we have provided novel evidence that reorganization (i.e., topographical shifts in peak activity) in the primary motor cortex after spinal cord injury is limited to individuals without neuropathic pain.