OBJECTIVE: To apply voxel-based methods to map the regional distribution of atrophy and T2 hyperintense lesions in the cervical cord of multiple sclerosis (MS) patients with different clinical phenotypes.
METHODS: Brain and cervical cord 3D T1-weighted and T2-weighted scans were acquired from 31 healthy controls (HC) and 77 MS patients (15 clinically isolated syndromes (CIS), 15 relapsing-remitting (RR), 19 benign (B), 15 primary progressive (PP) and 13 secondary progressive (SP) MS). Hyperintense cord lesions were outlined on T2-weighted scans. The T2- and 3D T1-weighted cord images were then analysed using an active surface method which created output images reformatted in planes perpendicular to the estimated cord centre line. These unfolded cervical cord images were co-registered into a common space; then smoothed binary cord masks and lesion masks underwent spatial statistic analysis.
RESULTS: No cord atrophy was found in CIS patients versus HC, while PPMS had significant cord atrophy. Clusters of cord atrophy were found in BMS versus RRMS, and in SPMS versus RRMS, BMS and PPMS patients, mainly involving the posterior and lateral cord segments. Cord lesion probability maps showed a significantly greater likelihood of abnormalities in RRMS, PPMS and SPMS than in CIS and BMS patients. The spatial distributions of cord atrophy and cord lesions were not correlated. In progressive MS, regional cord atrophy was correlated with clinical disability and impairment in the pyramidal system.
CONCLUSIONS:Voxel (unit of area see by MRI, like a computer pixel)-based assessment of cervical cord damage is feasible and may contribute to a better characterisation of the clinical heterogeneity of MS patients.
Using MRI they looked at the upper part of the spinal cord and found damage. At disease onset there was no obvious shrinkage of the spinal cord, as a marker of damage. In contrast PPMSers had more marked spinal nerve loss. There was some areas of damage in RRMSers, SPMSers and people with relatively benign disease. These were on the bottom and sides of the cord, where many of the movement-controlling nerves are. There was more damage in MSers with more active or long established disease. The areas of active lesions and nerve loss did not match in a snap shot, but they may not be expected to as lesions may only later equate to the nerve loss. In progressive MS there was nerve loss and the amount of nerve loss correlated with the degree of disability, notably movement nerve tracts (pryramidal system). This further confirmation of what we already thought