Clinical forms and course
Multiple sclerosis presents in various ways, which dictates the prognosis and treatment. The disease typically begins as a clinically isolated syndrome (CIS), the first episode of mono- or multifocal involvement (e.g., optic neuritis or transverse myelitis).
Main forms:
- Relapsing-remitting (RRMS): 85% of cases. Characterized by relapses alternating with complete or partial recovery of function.
- Secondary-progressive (SPMS): The inevitable outcome of RRMS in untreated patients (occurring in 50% of cases after years). Manifests as a steady accumulation of disability.
- Primary-progressive (PPMS): About 10% of cases. Characterized by progressive worsening from the outset, without distinct relapses. Less responsive to treatment due to a less prominent inflammatory component.
MRI diagnosis: McDonald criteria (2017)
MRI is the gold standard for detecting plaques. Diagnosis requires confirming two key principles: dissemination in space (DIS) and dissemination in time (DIT).
- Dissemination in space: presence of $\ge$1 T2 lesion in at least two of four specific areas: periventricular, cortical/juxtacortical, infratentorial, or spinal cord.
- Dissemination in time: simultaneous presence of gadolinium-enhancing and non-enhancing lesions, or the appearance of a new lesion on follow-up scans compared to a baseline scan.
Diagnosis of PPMS requires 1 year of clinical progression plus two of the following three criteria: brain lesions (in characteristic areas), $\ge$2 spinal cord lesions, or the presence of oligoclonal bands in the cerebrospinal fluid.
Characteristics of MRI lesions
Demyelinating lesions have specific features that help distinguish them from other pathologies.
- Location: Periventricular white matter (often oriented as "Dawson's fingers" perpendicular to the ventricles along veins), brainstem, cerebellum, spinal cord.
- T2/FLAIR: Lesions are hyperintense (bright), reflecting edema and demyelination. The volume of such lesions increases by 5–10% per year in the relapsing form.
- T1-weighted imaging: Some acute lesions appear dark ("wet black holes" — pronounced edema). Over time they may become isointense, but some progress to irreversible "chronic black holes" (severe axonal damage).
- Central vein sign: SWI sequence reveals a vein in the center of the lesion. This is an important marker for differential diagnosis.
- Enhancement: Gadolinium enhancement indicates active inflammation and blood-brain barrier breakdown (typically lasting up to 3 weeks). Incomplete (open) ring enhancement is characteristic.
Features of spinal cord involvement
Spinal cord lesions occur in 90% of multiple sclerosis patients. They are frequently localized in the cervical region.
On sagittal slices, these are "cigar-shaped" areas spanning no more than two vertebral segments. On axial slices, they are located in the lateral and posterior funiculi, occupying less than half of the spinal cord cross-section, and typically involve the central gray matter. Gadolinium enhancement is less common here than in the brain.
Briefly: answers to topical questions
What MRI modes and pulse sequences are included in the mandatory standardized diagnostic protocol for multiple sclerosis?
The sources list the following MRI modes and pulse sequences used in the evaluation of multiple sclerosis patients:
- T2/FLAIR — detects hyperintense white matter lesions.
- Contrast-enhanced T1-weighted imaging — detects gadolinium-enhancing lesions, indicating active inflammation and blood-brain barrier disruption.
- SWI — allows assessment of the central vein sign and the hypointense rim.
- 3D FLAIR, DIR, PSIR, MPRAGE — better visualize cortical lesions.
- PD and STIR — used to detect diffuse signal changes in the spinal cord.
Which diseases require differential MRI diagnosis with multiple sclerosis?
Differential MRI diagnosis of multiple sclerosis must be performed against a wide range of conditions that mimic its neuroimaging presentation.
- Neuromyelitis optica spectrum disorders (NMOSD) — distinguished by longitudinally extensive transverse myelitis.
- Acute disseminated encephalomyelitis (ADEM) — characterized by large, patchy lesions.
- Vascular pathologies — ischemic demyelination, infarctions, and primary angiitis of the CNS (PACNS).
- Autoimmune and granulomatous diseases — systemic lupus erythematosus (SLE) and neurosarcoidosis.
- Infections — HIV encephalitis and progressive multifocal leukoencephalopathy (PML).
- Metabolic disorders — vanishing white matter disease.
- Spinal cord tumors.
What cerebrospinal fluid (CSF) changes are characteristic of multiple sclerosis besides oligoclonal bands?
In the source for primary-progressive multiple sclerosis, an elevated CSF IgG index is listed as an additional CSF criterion; it may be considered alongside or instead of oligoclonal IgG bands.
Class and exam questions
What is the essence of dissemination in space and time?
Dissemination in space means the presence of lesions in different parts of the CNS (e.g., periventricular and in the spinal cord). Dissemination in time confirms that lesions did not appear simultaneously (e.g., presence of both old and new enhancing lesions).
What are "Dawson's fingers"?
These are ovoid demyelinating plaques in the periventricular white matter, oriented perpendicular to the walls of the lateral ventricles along the course of venules.
How to distinguish a multiple sclerosis lesion from a tumor based on enhancement?
MS lesions typically show incomplete (open) ring enhancement due to varying degrees of inflammation. In tumors and abscesses, the ring is usually closed.
Why does primary-progressive MS show fewer MRI changes yet progressive disability?
This is a clinico-radiological paradox. The reason lies in extensive yet standard-MRI-occult cortical damage, diffuse white matter injury, and predominantly spinal cord involvement.
What else to study on this topic
- Pathogenesis of neurodegeneration in multiple sclerosis
- Specific MRI sequences: SWI, DIR, PSIR
- Differential diagnosis with neuromyelitis optica spectrum disorders (NMOSD)
- Fulminant forms: Marburg, Schilder, and Balo diseases
- Tumefactive demyelinating lesions
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