Multiple sclerosis and neuroprotection: is laquinimod the answer?

Multiple sclerosis (MS) for most people engenders troublesome images of young people with disability, in wheelchairs, unable to care for themselves. The mere mention of the term elicits these fears. Surprisingly, the potential MS-mimic conditions tend to get a less fearful response. In my own practice, I have noticed that telling patients that their symptoms could be due to rheumatoid arthritis, Sjogrens Syndrome or systemic lupus erythematosus (SLE) does not have the same impact and yet we know that neurological involvement in those disorders can be disastrous, often much worse than MS.

So, why is it so? I guess MS is common and many people will know of someone or will have seen images of someone with MS, most of which will depict some degree of disability. Yes, MS is disabling but it is also now increasingly treatable, with numerous agents on the market and even more in clinical trials. The sobering aspect to most of this is that they all generally do the same thing-reduce clinical relapses and hopefully make the MRI scan look a little prettier. What does this do for long term disability? Well, we don’t really know. What we do know is that these drugs act by reducing inflammation but many years down the track, inflammation will stop and neurodegeneration will set in. We also now have increasing evidence that neurodegeneration-the process of gradual loss of brain cell populations-may start very early in the disease. The race is on to find a drug that can act on neurodegeneration, thereby stopping the very process that causes long-term physical disability.

In this issue of JNNP, there is a very interesting paper that provides a ray of hope in that regard. Fillipi and colleagues ( http://jnnp.bmj.com/content/85/8/851.abstract )have demonstrated that a new oral medication for MS, laquinimod, is associated with a reduction in the loss of brain volume that can accompany MS. This drug has been previously shown to reduce disability progression and this study was aimed at working out how it exactly did this. This is an important study as it is now widely accepted that loss of brain volume may be a marker of neurodegeneration and this measurement is now increasingly being used to assess the effectiveness of newer MS drugs.

What does this mean for patients? To answer that question, long-term follow-up will be needed focussing on patient-orientated parameters, particularly measures of physical function. In the meantime, this study provides hope that we may be entering an exciting new phase in the quest for effective treatments for MS.

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