On histologic examination, acute MS plaques show partial or complete destruction and loss of myelin with sparing of axon cylinders. They occur in a perivenular distribution and are associated with a neuroglial reaction and infiltration of mononuclear cells and lymphocytes. The perivascular demyelination gives the appearance of a finger pointing along the axis of the vessel. In the pathologic literature these elongated lesions have been named "Dawson's fingers." Active demyelination is accompanied by transient breakdown of the blood-brain barrier. Chronic lesions show predominantly gliosis. MS plaques are distributed throughout the white matter of the optic nerves, chiasm and tracts, the cerebrum, the brain stem, the cerebellum and the spinal cord. Endnote , Endnote

Imaging Features

      MS plaques are hyperintense on T2-weighted and FLAIR images and hypointense on T1-weighted scans. Specific signal intensities of MS lesions will vary depending on the magnetic field strength, the pulse sequence parameters, and partial volume effects. Occasionally, acute plaques may have a thin rim of relative T2 hypointensity or T1 hyperintensity. The T1 hyperintensity is attributed to free radicals, lipid-laden macrophages, and protein accumulations.

      MS plaques are usually discrete foci with well-defined margins. Most are small and irregular, but larger lesions can coalesce to form a confluent pattern. Multiple focal periventricular lesions can give a "lumpy-bumpy" appearance to the ventricular margins. As a result of their perivenular distribution, many periventricular plaques have an ovoid configuration, with their long axis oriented transversely on an axial scan. The ovoid lesion is the imaging correlate of "Dawson's finger." In general, MS plaques have a homogeneous texture without evidence of cystic or necrotic components. Hemorrhage is not a feature of MS lesions. Edema and mass effect are also uncommon.

      The periventricular white matter is a favorite site for MS plaques, particularly along the lateral aspects of the atria and occipital horns. The corpus callosum, corona radiata, internal capsule, visual pathways, and centrum semiovale are also commonly involved. When more than a few lesions are present, symmetric involvement of the cerebral hemispheres seems to be the rule. Any structures that contain myelin can harbor MS plaques, including the brain stem, spinal cord, subcortical U-fibers, and even within the gray matter of the cerebral cortex and basal ganglia. A distinctive site in the brain stem is the ventrolateral aspect of the pons at the fifth nerve root entry zone. Endnote Brain stem and cerebellar plaques are more prevalent in the adolescent age group. Endnote

      Lesions of the corpus callosum have been a special focus of study. On axial sections, plaques in the corpus callosum above the lateral ventricles have a transverse orientation along the course of the nerve fiber tracts and vessels. Sagittal FLAIR images are especially helpful to depict the small callosal lesions closely apposed to the superior ependymal surface of the lateral ventricles. Early edema and demyelination along subependymal veins produce a striated appearance. Atrophy of the corpus callosum is common in long-standing, chronic MS and is seen best on T1-weighted sagittal images.

      Involvement of the visual pathways, particularly the optic nerves, frequently occurs sometime during the course of disease. Patients may present with optic neuritis, although in about half of those cases, MRI will unveil other silent lesions in the brain. Imaging plaques in the optic nerves is a challenge even for MRI. Unenhanced spin-echo sequences are not very sensitive, and generally some type of fat suppression is required. Probably the most sensitive method for detecting acute MS of the optic nerves is the combination of gadolinium enhancement and fat suppression. Endnote

      The spinal cord is commonly involved by MS, and patients may present with a transverse myelitis. All levels of the cord can be affected, but most plaques are found in the cervical region. Since the white matter fiber tracts are positioned along the outer aspects of the cord, MS plaques are often based along a pial surface and have an elongated configuration. Signal characteristics are similar to lesions in the brain. Edema associated with acute plaques may lead to cord swelling, simulating an intramedullary tumor. In chronic MS, cord atrophy can result from focal lesions or axonal degeneration from distal disease. Endnote

      Nonenhanced MR cannot judge lesion activity, because plaques almost always remain evident after the acute clinical episode. Although the water content of acute plaques decreases over time, the T1 and T2 relaxation times of acute and chronic plaques have sufficient overlap that quantitative MR cannot distinguish between old and new lesions. Quantitative brain analyses of MS patients have shown that the T1 and T2 relaxation times are prolonged not only in acute and chronic plaques but also in normal-appearing white matter. Endnote Occasionally, a “dirty white matter” appearance can be seen on T2-weighted images. Diffuse white matter involvement has been confirmed further with magnetization transfer (MT) measurements. Endnote

      Gadolinium enhancement

      Since acute MS plaques are associated with transient breakdown of the blood-brain barrier, gadolinium contrast agents will produce enhancement of these lesions on T1-weighted images. Enhancement will be observed for 8 to 12 weeks following acute demyelination. Thus, Gd-enhanced MR can be used to assess lesion activity just like contrast-enhanced CT. Either nodular or ringlike enhancement may be seen early after contrast injection, but the central areas tend to fill in and become more homogeneous on delayed scans. Immediate postcontrast scans are most sensitive for detecting MS, and delayed scanning is not necessary. Contrast-enhanced MR can be used to follow the progression of disease and to assess the response to therapy. Endnote

      Occasionally, large plaques, also called tumefactive MS, may produce mass effect and simulate other mass lesions. However, compared with neoplastic or inflammatory processes, MS plaques have minimal surrounding edema and relatively less mass effect for the overall size of the white matter lesions. Balo's concentric sclerosis has a unique MR appearance. Like tumefactive MS, the plaques usually are quite large, but in addition, a concentric laminated pattern is seen on T2 and T1-weighted images. Similarly, post-contrast images often show rings of enhancement alternating with non-enhancing regions during the acute phase. Endnote  

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