Diagnosis

MRI has greatly enhanced the ability to establish a diagnosis early in the course of MS. This modality is noninvasive, reproducible, and sensitive to the presence or absence of disease and to both clinically evident and clinically silent changes in lesion burden. These features permit its use as a follow-up procedure to assess change.

An MRI is highly sensitive for the presence of disseminated white matter lesions. Gadolinium (GD) enhancement provides insights into active (enhancing) lesions because GD crosses into the CNS parenchyma only at sites of blood-brain barrier (BBB) leakage, whereas established inactive lesions do not show GD enhancement. New lesions often have central GD enhancement, whereas a ringlike or arcuate enhancement may be seen with reactivation at the margin of an existing plaque.

MRI may permit diagnosis during an initial clinical occurrence if the study demonstrates evidence of one or more lesions with dissemination in space and time, as illustrated by the simultaneous presence of GD-enhancing and nonenhancing lesions of typical configuration and location (periventricular, juxtacortical, infratentorial, or spinal cord). Diagnosis can also be established if a new T2 or GD-enhancing lesion, often clinically silent, appears on a follow-up MRI.

Classic MRI findings include so-called Dawson’s fingers, consisting of multiple well-demarcated ovoid perivenular plaques with their long axes situated perpendicularly within the corpus callosum and extending upward from the roof of one or both lateral ventricles, often as a fore and aft row situated parallel to the midline. Additional preferential plaque location sites include subcortical white matter, the middle cerebellar peduncles, the pons, and the medulla beneath the floor of the fourth ventricle. Spinal cord plaques originate at the meningeal surface and expand inward. Spinal cord plaques, as with plaques elsewhere, need not be symptomatic. Gray matter lesions within the cerebral cortex can be abundant in MS but are usually underappreciated because they are poorly visualized by standard MRI techniques. Rarely, white matter lesions can be ominously large, so-called tumefactive MS, and may even on occasion require biopsy to exclude glioma.

Up to 40% of time-spaced serial MRI scans demonstrate new GD-enhancing lesions in untreated patients with RRMS. Most such lesions are clinically silent. The finding indicates a several-fold higher level of disease activity than can be appreciated by considering overt clinical relapses alone. In contrast, the majority (60% plus) of randomly obtained MRI scans do not show current activity; this illustrates the presence of relative disease quiescence much of the time. However, this clinically inactive hiatus is intermittently interrupted by episodic pulses of MRI-detected or clinical MS disease activity. The frequency of MRI-positive newly active lesions is reduced by up to 80% by current treatments. GD-positive lesions are uncommon in progressive MS.

The validity of a diagnosis of MS based on the MRI criteria described above is established for RRMS in adults in Western countries. Criteria for a diagnosis of PPMS still require at least 1 year of disease progression plus two of three of the following criteria: (1) evidence for dissemination in space (DIS) from spinal cord into the brain based on at least one T2 lesion, not necessarily new, in a location characteristic for MS; (2) evidence for DIS in the spinal cord based on two lesions in the spinal cord; and (3) cerebrospinal fluid positive for oligoclonal bands, a positive immunoglobulin G (IgG) index (see later), or both.

MS is uncommon in children, and diagnosis at present requires a second attack to distinguish it from acute disseminated encephalomyelitis (ADEM), a distinct demyelinating disorder that is almost always monophasic (see later). MRI features that strongly favor the likelihood that a first attack of demyelinating illness will subsequently prove to be MS include presence of one or more T1-weighted hypointense lesions (black holes) indicative of prior CNS white matter damage or presence of one or more periventricular lesions. The likelihood for MS is further increased when both are present. In children younger than 11 years, MRI lesions are larger and more ill-defined than in teenagers or adults so that shape, size, and lesion frequency do not discriminate reliably between MS and ADEM, although a diffuse bilateral lesion pattern favors ADEM.

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