Abstract
Multiple sclerosis is a chronic demyelinating disease characterized by focal and diffuse inflammation of the central nervous system resulting in significant physical and cognitive disabilities. Disease-modifying therapies targeting the dysfunctional immune response are most effective in the first few years after disease onset, indicating that there is a limited time window for therapy to influence the disease course. No evidence of disease activity is emerging as a new standard for treatment response and may be associated with improved long-term disability outcomes. An aggressive management strategy, including earlier use of more potent immunomodulatory agents and close monitoring of the clinical and radiologic response to treatment, is recommended to minimize early brain volume loss and slow the progression of physical and cognitive impairments in patients with relapsing-remitting multiple sclerosis.
Highlights
Multiple sclerosis (MS) is a chronic demyelinating disease commonly ascribed to abnormal activation of autoaggressive T cells that cross the blood-brain barrier into the central nervous system (CNS) and result in demyelination and axonal loss
Diffuse inflammation is more pronounced in progressive forms of MS,[7,8] which may indicate secondary activation of the innate immune response and herald the onset of disability progression,[9] in which neurodegeneration resulting from inflammation predominates over focal inflammatory processes
Patients should be assessed for prior exposure to varicella zoster virus (VZV) before initiating fingolimod due to the risk of infection; vaccination is recommended in patients who are VZV antibody-negative
Summary
Multiple sclerosis (MS) is a chronic demyelinating disease commonly ascribed to abnormal activation of autoaggressive T cells that cross the blood-brain barrier into the central nervous system (CNS) and result in demyelination and axonal loss. As treatment effects may be delayed for several months after initiation, a brain MRI is advised 6 months after starting therapy This scan will serve as a new baseline for comparison with subsequent MRIs. The therapeutic response should be evaluated 6 to 12 months after the on-treatment reference scan, in accordance with Canadian treatment optimization recommendations.[94] Clear evidence of ongoing clinical or radiological disease activity in the first year of treatment should prompt a reexamination of the initial treatment choice and consideration should be given to employing a more potent agent. This approach has not yet been examined with alemtuzumab, and more data on the long-term efficacy and safety of induction strategies are required
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Schedule a callMore From: Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
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