MRI relapses have significant pathologic and clinical implications in multiple sclerosis.

MRI is extremely sensitive for detecting new inflammatory activity in the central nervous system of patients with multiple sclerosis (MS) that is often clinically silent. Each new lesion often leaves a permanent MS plaque, which is composed of varying degrees of demyelination, axonal loss, and gliosis. New large lesions have a greater risk of evolving into permanent T1-weighted hypointense lesions (black holes) that pathologically contain the greatest axonal loss and correlate more strongly with clinical disability than with overall lesion load on T2-weighted images. There is also an association between the severity of the total T2 lesion burden with cerebral atrophy and with diffuse changes in the normal-appearing brain tissue as determined by magnetization transfer imaging and magnetic resonance spectroscopy. To maintain normal clinical functioning, the brain may compensate by recruiting increased regions of cortex, as demonstrated by functional MRI (fMRI) studies. The degree of increased fMRI activation is proportional to the severity of T2 lesion load, up to a critical limit at which it appears that these compensatory mechanisms may fail. Therefore, new inflammatory activity, as detected by MRI, carries a risk of significant early pathologic damage and delayed yet permanent clinical disability.