When cells, total protein, gamma globulin, and oligoclonal bands are all taken into account, some abnormality of the spinal fluid will be found in the great majority of patients with established MS. At present, the oligoclonal bands in the CSF is the most widely used of the CSF tests for MS, particularly when taken some interval after an acute exacerbation or during the chronic progressive phase of disease. The more complicated laboratory procedures, such as CSF measurements of globulin production or MBP provide little additional sensitivity.
It is now widely appreciated that MRI is the most helpful ancillary examination in the diagnosis of MS, by virtue of its ability to reveal symptomatic and asymptomatic plaques in the cerebrum, brainstem, optic nerves, and spinal cord (see Fig. 35-1). Most experience indicates that the incidence of MRI lesions in the cerebra and spinal cord is greater than 90 percent in established cases of MS. While the majority of cerebral lesions tend to be asymptomatic, spinal cord lesions are almost always symptomatic.
Several MRI features are characteristic of the MS lesion. In general, MS plaques are hyperintense (white) on T2-weighted images and even more obvious on T2 fluid-attenuated inversion recovery (T2-FLAIR) images. The T2 sequence is particularly sensitive in detecting lesions in the brainstem, cerebellum, and spinal cord. Acute lesions tend to demonstrate tissue expansion due to edema that is evident as T1 hypointensity and T2 hyperintensity. Chronic lesions, in distinction, are usually contracted and hyperintense on T2 sequences. The presence of T1 hypointensity depends on the extent of remyelination of the lesion. If there is no or scant remyelination, the center of the chronic lesion gives the appearance of a “black hole.” As assessed histologically with both autopsy and MRI studies, T1 hypointensity was inversely proportional to the degree of remyelination (Barkhof et al).
While the finding of individual cerebral lesions on MRI do not always ensure the diagnosis of MS, the finding of multifocal, well-demarcated, oval or linear, radially oriented lesions adjacent to the ventricular surface are fairly specific for typical relapsing-remitting form of MS (Fig. 35-1, left panel). When viewed in sagittal images, they extend from the corpus callosum in a filiform pattern and have been termed “Dawson fingers.” The radial orientation of these lesions corresponds to the course of venules embedded within the cerebral white matter. In addition to these periventricular lesions, subcortical and infratentorial lesions are frequently seen, most often in white matter tracts such as the cerebral and cerebellar peduncles and the medial longitudinal fasciculus. Lesions in MS do not conform to cerebral vascular territories and lack the wedge shape of typical embolic cerebral infarctions. Diffusivity in MS lesions is variable, but can be a feature of larger, acute lesions.
Early in the evolution of an MS lesion, there is disruption of the blood–brain barrier, presumably as a consequence of inflammation. The MRI correlate of this inflammation is abnormal enhancement following the administration of gadolinium. Gadolinium enhancement may last for many weeks. One characteristic pattern is of a C-shaped partial or open ring of abnormal enhancement, which assists in differentiating a MS plaque from other lesions such as abscess and neoplasm. The open segment of the ring is most often medially situated. Many of these imaging characteristics are listed in Table 2-3 and displayed in Fig. 35-1.
In advanced cases of MS, the periventricular lesions may become confluent, usually at the poles of the ventricles. Infrequently, a large acute lesion may have a mass effect and a ring-like contrast-enhancing border, then resembling a glioblastoma or an infarct—the previously referred to “tumefactive” lesion (see Fig. 35-2).