Multiple Sclerosis: A Therapeutic Overview

Mark H. J. Litzinger, BSc, BSc Pharm, RPh; Monica Litzinger, BSc, BSc Pharm, RPh


US Pharmacist. 2009;34(1):HS3-HS9. 

In This Article


Multiple sclerosis (MS) was first described over 100 years ago, yet it remains unfamiliar to many clinicians.[1] MS is a chronic neurologic disorder that affects the central nervous system (CNS).[2] It is characterized by the impairment of nerve transmission down the axon, attributed to chronic unpredictable inflammation and demyelination of neurons.[3] In other words, unusual lesions damage the protective coat (myelin) of nerve fibers, thus inhibiting the messages sent within the brain and to the spinal cord. Clinical presentation of MS is associated with exacerbations of weakness, imbalance/incoordination, spasticity, fatigue, bladder/bowel difficulties, vision loss, altered sensory perception, cognitive impairment, and neuropathic pain.[4] Such signs and symptoms have a broad differential diagnosis, and therefore diagnosing MS is difficult when they initially present as an isolated clinical event. However, the clinical course over time--multifocal attacks, with an increasing burden of new demyelinative lesions seen on MRI scans and characteristic cerebrospinal fluid (CSF) findings--enable the diagnosis to be made.[5] Furthermore, there is no single test for MS, and diagnosis is based on a history of attacks (i.e., at least one month apart) and myelin destruction in more than one area (i.e., brain and spinal cord).

The treatment of MS is limited to treating exacerbations, managing symptoms, improving function, and using disease-modifying drugs (DMDs). Treatment efforts are utilized in an attempt to improve the patient's quality of life. The cost of therapy can be substantial, since insurance companies may not cover the cost of DMDs without a firm diagnosis of clinically definite MS. The use of DMDs results in fewer new demyelinative lesions over time, but progressive neurologic disability is common, particularly when axonal degeneration occurs in response to chronic ongoing inflammation within the adjacent myelin sheath.


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