A definitive diagnosis of multiple sclerosis is based on a combination of the neurological signs and symptoms, laboratory findings and magnetic resonance imaging (MRI). Following the McDonald Criteria is a helpful tool in the diagnosis of multiple sclerosis. Utilizing this, aids in differentiating between relapse-remitting disease and progressive disease versus having a clinically isolated syndrome (CIS).
Because symptoms can be very broad, depending on the effected areas of the brain, a thorough neurological exam is key. Some of the most common initial presentation of symptoms include weakness, numbness, tingling, unsteadiness in a limb; spastic paraparesis; optic neuritis; diplopia; disequilibrium; or sphincter disturbance resulting in urinary urgency or hesitancy (Aminoff & Douglas, 2017). Obtaining a history of onset and evolution of symptoms is essential in determining whether a clinically isolated syndrome is occurring versus a relapse or due to progressive disease (Brownlee, Hardy, Fazekas, & Miller, 2016).
Laboratory findings of cerebrospinal fluid (CSF) are not often essential in but are helpful in supporting the diagnosis of multiple sclerosis (Brownlee et al., 2016). Common findings in CSF include (Brownlee et al., 2016):
- slightly elevated WBC
- presence of proteins
- elevated IgG index
- presence of oligoclonal bands
An abnormal brain MRI is standard in the diagnosis of MS; however, obtaining an MRI of the brain and spinal cord is important to eliminate other plausible disease processes (Brownlee et al., 2016). The diagnosis of multiple sclerosis requires objective evidence of CNS lesions disseminated in time and space (Brownlee et al., 2016). This means that two separate attacks with signs of two or more lesions must found based on clinical findings (Brownlee et al., 2016).
Figure 1. Brain and Spinal Cord MRI (Brownlee et al., 2016)
Figure 2. McDonald Criteria (Brownlee et al., 2016)
Treatment is currently aimed at the prevention of acute relapses that, in time, lead to the accumulation of disability (Aminoff & Douglas, 2017). The long-term treatments include injectable and oral immunomodulary drugs such as:
During an acute relapse, corticosteroids, such as methylprednisone, are often used due to their own immunosuppressive and anti-inflammatory properties. During severe exacerbations, when corticosteroids are not adequate enough, plasmapheresis can be considered (Garg & Smith, 2015).
Other treatment modalities are aimed at symptom management during acute relapses, and supportive and rehabilitative management to help with complications from immobility (McCance & Huether, 2014).