Abstract

Multiple sclerosis (MS) is a damaging CNS disease. Because the CNS has inherent properties that prevent the damage from manifesting readily (e.g., redundancy, plasticity, repair), often irreversible damage is not appreciated until very late. Pathologically it is apparent that permanent and irreversible damage occurs very early in MS plaque formation.1 Treatment of the disease course can therefore be viewed as having 3 goals: 1. Damage control to prevent or limit further damage 2. To protect injured axons and neurons from further injury 3. To encourage repair of reversibly damaged tissue It is clear that once patients are diagnosed with MS, or at high risk of developing MS (clinically isolated syndrome), they have already sustained damage to their CNS. How much damage it takes before patients actually present is variable: it is astounding at times to see patients even after one attack who have accumulated substantial disease loads on their MRI scans or already demonstrate symptoms and signs of chronic disease, such as cognitive or even physical impairment. It can be argued that current therapies are inadequate for some of these patients, though the goals of therapy are still probably reasonable but more difficult to realize. Once a patient enters the progressive phase of illness, with few relapses and minimal activity on MRI, it may be too late with our current armamentarium of agents to attain any of the stated goals of treatment. The exact etiopathogenesis of damage in MS is still …

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