Introduction

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system affecting nearly 350,000 people in the United States and an estimated two million people worldwide. It is the most common cause of non-traumatic neurologic disability in young and middle aged adults1. The etiology is unknown, although the disease commonly is regarded as an autoimmune process triggered in susceptible individuals by an early environmental exposure.

Clinically MS is characterized by attacks of neurologic dysfunction, which may be few and far between with little or no impact on a person's ability to function. At times though, they may cause a rapid deterioration leading to complete disability. Most people with MS fall between these extremes. Most MS patients live for decades after their diagnosis. MS reduces life expectancy after onset by about 6-7 years2, and about half of the patients survive 30 years or more from onset3.

In the past few years, progress in MS research has accelerated. Novel approaches have elucidated many aspects of its pathophysiology. For example, genetics of susceptibility, identification of myelin antigens, inflammation, the roles of T-cells macrophages and astrocytes, mechanisms of demyelination and limited remyelination have all been under focus. Disease modifying drugs such as interferon beta and glatiramer acetate exert documented, albeit modest, effects during attacks in relapsing-remitting MS and are now widely used.

In addition, renewed interest in axonal damage in MS has opened new directions to approach the understanding and treatment of this disorder. Although MS is primarily an

Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195; Email, [email protected].

inflammatory demyelinating disease, it has become evident that axonal degeneration plays an important role in the pathogenesis of disability for MS patients4-8. More import-tantly axonal transection has been shown to begin at disease onset9, but remains clinically silent probably due to the brain's remarkable plasticity in the face of injury. Considering the role of axonal injury in the pathogenesis of MS, non-invasive axonal monitoring could be used for prognostication, for the study of disease progression, as well as for evaluation of ongoing therapy. In vivo magnetic resonance spectroscopic determination of W-acetyl-L-aspartate (NAA), a specific neuronal/axonal marker, may provide such a measure10' 11. This chapter reviews current data on axonal pathology and the role of NAA in MS.

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