The most obvious impairments associated with spinal cord injury (SCI) are loss of sensation and motor control. However, many subjects with SCI also develop persistent neuropathic pain below the injury which is often severe, debilitating and refractory to treatment. The underlying mechanisms of persistent neuropathic SCI pain remain poorly understood. Reports in amputees describing phantom limb pain demonstrate a positive correlation between pain intensity and the amount of primary somatosensory cortex (S1) reorganization. Of note, this S1 reorganization has also been shown to reverse with pain reduction. It is unknown whether a similar association between S1 reorganization and pain intensity exists in subjects with SCI. The aim of this investigation was to determine whether the degree of S1 reorganization following SCI correlated with on-going neuropathic pain intensity. In 20 complete SCI subjects (10 with neuropathic pain, 10 without neuropathic pain) and 21 control subjects without SCI, the somatosensory cortex was mapped using functional magnetic resonance imaging during light brushing of the right little finger, thumb and lip. S1 reorganization was demonstrated in SCI subjects with the little finger activation point moving medially towards the S1 region that would normally innervate the legs. The amount of S1 reorganization in subjects with SCI significantly correlated with on-going pain intensity levels. This study provides evidence of a link between the degree of cortical reorganization and the intensity of persistent neuropathic pain following SCI. Strategies aimed at reversing somatosensory cortical reorganization may have therapeutic potential in central neuropathic pain.

Cohort of incident cases from 1955 to 2006. To analyse acute and long-term mortality, estimate life expectancy and identify survival patterns of individuals experiencing traumatic spinal cord injury (SCI). Specialised SCI unit in Australia. Data for patients with traumatic SCI admitted to a spinal unit in Sydney, Australia between January 1955 and June 2006 were collated and deaths confirmed. Cumulative survival probability was estimated using life-table techniques and mortality rates were calculated from the number of deaths and aggregate years of exposure. Standardised mortality ratios (SMRs) were estimated from the ratio of observed to expected number of deaths. Life expectancy was then estimated using adjusted attained age-specific mortality rates. From 2014 persons, 88 persons with tetraplegia (8.2%) and 38 persons with paraplegia (4.1%) died within 12 months of injury, most often with complete C1–4 tetraplegia. Among first-year survivors, overall 40-year survival rates were 47 and 62% for persons with tetraplegia and paraplegia, respectively. The most significant increases in mortality were seen in those with tetraplegia and American Spinal Injury Association Impairment Scale (AIS) grades A–C lesions, with SMRs between 5.4 and 9.0 for people 50 years, reducing with advancing attained age. Estimated life expectancies from 25 to 65 years ranged between 69–64%, 74–65%, 88–91% and 97–96% for C1–4 AIS A–C, C5–8 A–C, T1–S5 A–C and all AIS D lesions, respectively. Survival related strongly to extent of neurological impairment. Future research should focus on identifying contextual factors, personal or environmental, that may contribute to the reduced life expectancy after SCI.