General description

Multiple sclerosis (MS) is a primary demyelinating disease caused by autoimmune etiology, characterized by periventricular, juxtacortical, infratentorial, and spinal cord plaques. Plaques are associated with macrophage infiltration, lymphocyte perivascular cuffing, fibrin accumulation and reactive microglia. Iron deposits also can be found in MS.

McDonald criteria

Oligoclonal bands

MS presents with a single clinically isolated syndrome (CIS). In patients with CIS, MS can be diagnosed without dissemination in time (DIT) on MRI if the oligoconal bands are positive and there are no atypical findings on CSF examination.

Dissemination in space (DIS) and time (DIT)

The McDonald criteria necessitate the presence of at least one white matter hyperintensity in a minimum of two characteristic locations, including periventricular, juxtacortical, infratentorial regions (such as the brainstem), and the spinal cord, to demonstrate dissemination in space (DIS).

Dissemination in time (DIT) is indicated by the coexistence of lesions with and without contrast enhancement at any point, or by the appearance of new high-signal lesions on T2WI or lesions with contrast enhancement during follow-up MRI.

Radiographic features

Ovoid lesion/Dawson fingers

Circular or oval foci are primarily observed in the periventricular white matter of the lateral ventricles, brainstem, cerebellum, and other cerebral white matter. However, MS lesions can be located throughout the brain, with potential involvement of cortical regions and the basal ganglia.

The ovoid shape of lesions in MS is indicative of the course of the inferior ependymal vein, a characteristic feature of the disease. Periventricular lesions with ovoid shape and perpendicular to the ventricle are called Dawson fingers. The lesions are often in contact with the ependyma, which is useful in differentiating them from ischemic changes. They may also be found around the temporal pole near the inferior horn of the lateral ventricle, which is also useful in differentiating them from ischemic changes, since they are not often seen in ischemic changes.

T2*WI and SWI may also be useful for identifying central veins. Central vein sign detected by SWI at MRI is a good discriminator between ovoid lesion and leukoaraiosis.

Septal-callosal interface lesion

Lesions located within the corpus callosum, oriented perpendicular to the ventricles, are considered a hallmark of MS. The corpus callosum is typically resistant to ischemia and is rarely affected by cerebrovascular disease or vasculitis, making it a valuable anatomical site for differentiating MS from other conditions. Lesions in the corpus callosum are observed in 55-95% of MS cases. Additionally, atrophy of the corpus callosum has been associated with cognitive dysfunction and progression of the disease.

Dot-Dash sign can be visualized as an irregularity of this ependymal stripe on the undersurface of the corpus callosum, defined by at least 2 “dots” connected by a “dash”.

Juxtacortical lesion

In MS, the cortical to subcortical U-fiber region (juxtacortical white matter) is commonly affected, a feature considered characteristic of the disease. This subcortical U-fiber is typically spared in ischemic lesions, as it receives blood supply from both the medulla and cortex. Its involvement in MS may reflect underlying perivascular inflammation.

T1-weighted imaging

It is important to recognize that T1WI hypointense lesions in MS have different implications depending on the disease phase. In the chronic phase, T1WI hypointense areas, referred to as T1 "black holes," are indicative of axonal loss. Conversely, in the acute phase, such lesions typically reflect edematous changes associated with inflammation. While necrotic areas due to ischemia also present as T1WI hypointense, they remain consistently higher in signal intensity than cerebrospinal fluid (CSF) in MS, whereas ischemic necrotic tissue has a signal intensity nearly equal to that of CSF. A point of differentiation from MS is acute disseminated encephalomyelitis (ADEM), a condition that rarely exhibits T1 "black holes."

Contrast effect

In MS, contrast enhancement is observed in active lesions and is useful in assessing dissemination in time (DIT). The pattern of contrast enhancement can vary, presenting as either homogeneous or ring-shaped. The ring-shaped enhancement is particularly indicative of myelin sheath loss and surrounding inflammation. Among the ring-shaped contrast effects, those that are defective on the gray matter or basal ganglia side are called open ring signs, and are characteristic of demyelinating diseases such as MS.

Infratentorial lesion

Brainstem lesions in MS are typically peripheral, asymmetric, and unilateral. Cerebellar lesions are usually located in the middle cerebellar peduncle, although inferior and superior cerebellar peduncles and cerebellar hemispheres may also be affected.

Optic nerve involvement

Optic neuritis in MS is typically acute onset and unilateral. In the acute phase of optic neuritis, the optic nerve is enlarged, showing high signal on STIR and contrast effects within the optic nerve. The contrast effect suggests disruption of the neuroblood barrier, and coronal sections show a uniform contrast effect over the entire optic nerve.

Spinal lesion

MRI reveals swellings and T2-weighted hyperintensity affecting the lateral and posterior columns, with a typical lesion length of less than the height of two vertebral bodies. In contrast, Neuromyelitis optica spectrum disorder (NMOSD) typically involves lesions extending over more than three vertebral bodies. This distinction serves as an important differential point between MS and NMOSD.