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During the years of treatment, patients exhibited signicant atrophy and did not; in the former group, experienced an increase in Endurobol disability whereas in the latter group only became more disabled.Prolonged year followup of some of the placebo cohort from this trial assessed the longer term relationship between earlier BPF change and later disability.Comparison of patient quartiles based on change in BPF over the rst years revealed a greater likelihood of developing severe disability in those with the most atrophy during the initial years.More recently, progressive cerebral and cervical cord atrophy has been observed over years of followup in a cohort of primary progressive MS patients.The rates of atrophy appeared to be relatively constant within individual patients but varied between subjects.A study of patients with primary progressive MS evaluated riluzole, a neuroprotective glutamate antagonist, using change in cord area as a putative measure of progressive Fluoxetine axonal loss.During year pretreatment, there was a reduction in mean cord area whereas during year on treatment the cord area was stable, but the difference was not signicant.This preliminary study indicates the potential of using tissue volume measures in larger cohorts to study the efcacy of neuroprotective agents.A recent review discusses in depth the methodological and clinical aspects of atrophy in MS.A reduction in NAA provides evidence of axonal dysfunction or loss and has been consistently reported in MS lesions and NAWM.A greater reduction of NAWM NAA is observed in secondary and primary progressive than in relapsing remitting MS, and disability has been correlated with reduced NAA in both cerebral, and cerebellar NAWM.Decreased NAA has also been observed in cortical gray matter in early relapsing remitting MS, suggesting that early neuronal cell body damage is occurring.It is reduced by in thalamic gray matter in secondary progressive MS and in a postmortem study the decrease in NAA was associated with decreased numbers of neurones.In primary progressive MS, reduction of NAA and atrophy appear to be relatively independent of T lesion load.This has been reported to be low in patients with CIS.The resonance for wholebrain NAA is broad and requires manual delineation for quantication; its analysis is potentially subject to bias and poor reproducibility.In contrast, the narrow NAA resonances from small voxels, obtained as a single region or as part of a spectroscopic imaging slice, can be automatically identied and quantied with a model that uses as reference a solution with a known concentration of NAA.A limitation of spectroscopy is the low signaltonoise ratio and modest reproducibility of the measured metabolite concentrations.For this reason, it has been little used in multicenter therapeutic trials.Two small singlecenter studies of patients treated with interferon have produced conicting results.One study showed an increase in NAA, suggesting a therapyinduced reversal of axonal dysfunction.The other showed a decrease in NAA, suggesting that progressive axonal loss continues in spite of treatment.In spite of methodological difculties, more vigorous efforts to investigate NAA as a surrogate outcome in trials of neuroprotection in MS would seem warranted, given that this metabolite provides specic information on axonal survival and function.

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