Over the past decade, modern structural magnetic resonance imaging (MRI) techniques have been extensively used for the study of patients with multiple sclerosis (MS).¹ The ultimate goal of this research is to increase the understanding of the mechanisms responsible for the accumulation of irreversible disability. Although important insight into MS pathobiology has been achieved by using modern MR based techniques, the magnitude of the correlation between MRI and clinical findings remains suboptimal. This might be explained, at least partially, by the variable effectiveness of reparative and recovery mechanisms following MS related tissue damage.

Resolution of acute inflammation, remyelination, and redistribution of voltage gated sodium channels in persistently demyelinated axons are all likely to limit the clinical impact of damaging MS pathology.² Cortical reorganisation has been recently suggested, however, as an additional potential contributor to the recovery or to the maintenance of function in the presence of irreversible MS related tissue damage. This is in agreement with what has been seen in other neurological conditions, such as stroke,³ tumours,^4,5 and Alzheimer’s disease.^6,7 Brain plasticity is indeed a well known feature of the human brain, which is likely to have several different substrates (including increased axonal expression of sodium channels,⁸ synaptic changes, increased recruitment of parallel existing pathways or “latent” connections, and reorganisation of distant sites), and which might have a major adaptive role in limiting the functional consequences of axonal loss in MS.⁹

What is measured using fMRI?

The signal changes seen during functional MRI (fMRI) studies depend on the blood oxygenation level dependent mechanism, which, in turn, involves changes of the transverse magnetisation relaxation time—either T2* in a gradient echo sequence or T2 in spin echo sequence.⁵ Local increases in neuronal activity result in a rise …