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Arch Neurol. 2001;58:30-32.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

THE STUDY of multiple sclerosis (MS) has been one of the more active and rewarding areas of neurological research in the last quarter of the 20th century. Viewed as the pathological consequence of a partially dysregulated immune response turned against certain myelin components, MS has recently joined the growing forefront of neurological illnesses for which disease-modifying treatments are now available. Yet, the continued advancement of better and more effective therapies relies on a better understanding of the pathological basis of MS, especially in relation to its associated neurological consequences.

The most apparent aspects of MS in most individuals are relapses and a subsequent irreversible worsening (progression) of neurological deficits. Generally, clinical relapses have been considered to be associated with sporadic focal inflammatory events within clinically eloquent areas of the brain and spinal cord, while the sustained progression of clinical disability has been associated with accumulated, relapse-associated, focal myelin and axonal . . . [Full Text of this Article]

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