Multiple sclerosis (MS) is the main cause of non-traumatic chronic disability in young adults with neurological disorders (Ramagopalan and Sadovnick 2011). Clinical manifestations are provoked by multifocal demyelination and axonal damage in multiple areas of the CNS, causing functional deficit or negative symptoms; positive symptoms completing the clinical spectrum include neuropathic pain and paroxysmal phenomena resulting from inappropriate axon response (Smith and McDonald 2003).
MS presents as one of four distinct clinical variants or forms: relapsing remitting, primary progressive, secondary progressive, or progressive relapsing. Approximately 87 percent of patients show the relapsing remitting form, characterized by acute attacks (relapses), followed by partial or full recovery (remissions) (Weiner 2008). Patients can manifest with a heterogeneous group of symptoms, including changes in vision, lack of coordination, sensory distortion or loss, or changes in bowel or bladder function.
Specific immunomodulatory therapies have shown significant impact on MS natural history. However, even when agents reduce relapse rates and MRI-associated disease activity, they are only partially effective, and do not ameliorate the irreversible axonal damage underlying the most significant symptomatic burden. MS-associated symptom treatment remains an essential cornerstone of comprehensive care for affected patients.