ABSTRACT
Demyelination is the pathologic hallmark of the multiple sclerosis (MS) lesion and has long been believed to be the underlying cause of neurologic deficits. However, demyelination is accompanied by varying degrees of inflammation, oligodendrocyte death, axonal loss, complement activation, antibody deposition, and gliosis (1-4). With the development of magnetic resonance imaging (MRI) patients who present with minimal or no neurologic deficits are routinely identified with extensive white matter lesions. Pathologic examination of central nervous system (CNS) tissue at biopsy or autopsy has confirmed that lesions visible by MRI were demyelinated and often involved substantial areas of the CNS that should have resulted in neurologic deficits (5). It is now clear that loss of axons is the ultimate cause of permanent disability rather than demyelination.
