As discussed below, in recent criteria for diagnosis, and in keeping with the traditional notion of MS as a disease that is “disseminated in time and space,” the MRI is invaluable for demonstrating asymptomatic lesions. It is the discovery of these additional lesions in a patient with a single clinical episode that can establish the diagnosis of MS. Similarly, the unsuspected diagnosis of MS may be revealed on a single MRI by detecting 1 or more acute, enhancing lesions with additional nonenhancing ones. Some of these asymptomatic lesions may be found in the spinal cord, as discussed by Bot and colleagues. Furthermore, serial MRIs showing accumulating T2 hyperintense lesions over time are consistent with the diagnosis. As with other laboratory procedures, MRI changes assume maximal significance when they are consistent with the clinical findings.
Less evident than the focal lesions of MS is the progressive cerebral atrophy that accompanies most cases. This change probably reflects both the loss of glial cells and, importantly, wallerian degeneration and loss of axons triggered acutely by inflammation and more chronically by other neurodegenerative processes (Miller et al, 2002). Several studies document that slowly progressive brain atrophy, as gauged by volumetric MRI measurements of the cortical mantle, deep nuclei, and white matter, is a feature of MS. This is demonstrable both early and late in the disease and correlates particularly with cognitive disability.
The spinal lesions of MS occupy only a portion of the transverse surface of the cord, most commonly being situated in white matter tracts in a subpial location. The lesions infrequently extend longitudinally beyond three contiguous vertebral segments (see Fig. 35-1), in contrast to those of NMO as discussed in the following text. As described above, acute lesions may cause focal expansion of the cord and enhance with contrast, while chronic lesions tend to produce atrophy.
It should be stressed that foci of periventricular T2 hyperintensity are observed with a variety of pathologic processes and even in normal persons, particularly older ones. Unlike the lesions of MS, these periventricular lesions are usually oriented parallel to the ventricular surfaces, are smoother in outline than the lesions of MS, and have been attributed to microvascular changes (as discussed in
Chap. 33). The same lack of specificity of cerebral lesions pertains to those in the spinal cord.
CT may also demonstrate cerebral lesions, sometimes unexpectedly, but with far less sensitivity than MRI. Two points worth noting about the CT are that acute plaques can appear as contrast-enhanced ring lesions, simulating abscess or tumor, and that some contrast-enhanced periventricular lesions become radiologically inevident after steroid treatment.
When the clinical and radiographic data point to only one definite lesion in the CNS, as often happens in the early stages of the disease or in the spinal form, a number of other sensitive physiologic tests may establish the existence of additional asymptomatic lesions. These include visual, auditory, and somatosensory-evoked responses; electromyographic evaluation of the blink reflex; and measurement of subjective visual flicker fusion. Abnormalities of visual evoked responses have been found in approximately 70 percent of patients with the clinical features of definite MS and 60 percent of patients with probable or possible MS. The corresponding figures for somatosensory evoked responses have been 60 and 40 percent, and for brainstem auditory evoked responses (usually prolonged interwave latency or decreased amplitude of wave 5), approximately 40 and 20 percent, respectively (see
Chap. 2). These tests had been used with greater frequency in the past and have been largely supplanted by MRI to detect dispersed demyelinating lesions.
Optical coherence tomography (OCT) is a technique that measures the back-scattering of near-infrared light to create extremely high resolution cross-sectional images of the optic nerve and retina. Automatic segmentation of the retinal nerve fiber layer thickness allows accurate, reliable quantification of axonal loss and thinning over time that follows optic neuritis.