It is a chronic, progressive autoimmune disease of the central nervous system, manifested by diffuse neurological symptoms and having a relapsing-remitting course in its initial stages in typical cases (Adams and Victor 1993). The history of the disease study begins in 1835, when the French pathologist J. Kruvelie described “spotted” or “insular” sclerosis. MS is considered the best understood in the group of demyelinating diseases, but its etiology is still unclear. Etiological hypotheses consider an infection, autoimmunity to normal myelin, a combination of infectious and autoimmune processes, and toxic and metabolic causes of MS. Currently, the most common is the hypothesis of multifactorial etiology of MS, according to which the disease develops, when a certain combination of external factors affects genetically susceptible individuals, causing chronic inflammation, autoimmunity, and demyelination of the white matter in the CNS. The genetic predisposition to MS remains unproven; however, the development of MS has been established to be most strongly associated with HLA class II DR2 haplotype. The role of other genes in the etiology of MS, as well as the possibility of a combination of different genetic factors, is still discussed.

In the majority of cases, these lesions have a relatively homogeneous MR signal and clear limits with the white matter. The form of MS plaques may be the most diverse, varying from round to irregular one. However, rounded lesions are encountered more often; they are identified mainly in the periventricular region and semioval centers and less frequently in the corpus callosum and subcortical structures. Individual plaques can be located in the projection of the brainstem and cerebellar hemispheres. On T1-weighted MRI, in relapsing-remitting MS, the plaques are not visible in most cases and only individual lesions are identified, which are characterized by a slightly hypointense MR signal. This group is also characterized by the absence of visualization of subtentorial plaques in T1-weighted images.

MS plaques may accumulate the contrast agent, reflecting transient BBB disorders. Contrast enhancement is used in MS to identify more or less specific features in the hyperintensity picture of multiple foci in T2-weighted images. It is known that the simultaneous detection of both contrast-enhanced and non-contrast-enhanced lesions is a characteristic of MS and puts in question other diagnoses (Fig. 41.1).

The diffuse type of contrast enhancement is characterized by opacification of an entire plaque. This type of contrast enhancement is a characteristic for multiple, small demyelination foci (a few millimeters in size). The annular type of contrast enhancement is observed with the accumulation of contrast agent in peripheral portions of larger foci—in the form of a ring. The dimensions of these lesions usually approach 1 cm or more. This type of contrast enhancement is a characteristic for plaques with the presence of a perifocal edema detectable in T2-weighted and DW images. This partial type of contrast enhancement, from our point of view, is the most pathognomonic for demyelination foci in MS, in general, and is manifested in the form of partial CA accumulation within the area of abnormal changes in the intensity of an MR signal detected by T2-weighted MRI. At the same time, the attention should be drawn to contrast enhancement of MS plaques in the form of a “half-ring” or a “half-moon,” when an increase in the MR signal intensity on post-contrast T1-weighted images is observed only in a limited area on the plaque periphery, not confined to annular opacification (Fig. 41.2).