MRI features of demyelination:
Demyelinating lesions can be broadly classified into grey matter, white matter, optic nerve and spinal cord lesions.
White matter lesions are the most common lesions found in demyelinating disorders. These lesions appear hyperintense on T2WI. While this is a sensitive finding, it is hardly ever specific if taken in isolation. FLAIR sequences improve tissue contrast by suppressing the signal from CSF, making juxtacortical lesions easier to identify.
T1WI can initially appear normal, however in some patients the plaques appear hypointense. These lesions can be either acute or chronic and represent axonal injury.
Gadolinium based imaging can help distinguish between active and chronic lesions. These lesions can be homogenous, heterogenous or ring enhancing. Lesions that are seen on T2WI and T1WI that also show gadolinium enhancement are acute in nature. However, it is important to note that Gadolinium enhancement of white matter lesions may not completely correlate with clinical presentation as Gadolinium enhanced imaging is 5-10 times more sensitive at identifying active inflammatory lesions.
Grey matter lesions are classified into subcortical and cortical lesions. T2WI is relatively insensitive in identifying grey matter plaques. On T2WI, hypointensities of grey matter are observed, particularly in the subcortical grey matter. Double Inversion Recovery and FLAIR have a higher sensitivity compared to T2WI in identifying white matter lesions.
Spinal cord lesions are best visualized on T2WI and STIR/FSE sequences. Demyelinating lesions appear as hyperintense, however can be missed if are very small. Similar to white matter changes, T1 hypointensities can also be seen within the spinal cord.
Optic nerve involvement is best demonstrated with dedicated imaging of the optic nerve. STIR sequences play a role in facilitating identification of plaques over the optic nerve. Advanced imaging techniques like diffusion tensor imaging are also used in certain circumstances, however, provide no significant diagnostic advantage. Like white matter lesions, these plaques also demonstrate gadolinium enhancement.13
Features of demyelinating disorders on MRI:
Although there is cross-over among the different disorders, each disorder is associated with certain unique pattern of imaging findings.
In patients with MS, unilateral optic neuritis, short longitudinal cervical spinal cord lesions, periventricular (Dawson’s fingers - Fig 1 and 2), juxtacortical and posterior fossa involvement is commonly seen. Optic neuritis in MS is typically unilateral, short and involves minor extension into the chiasm (Fig 3). The spinal cord lesions are short and hence are often missed. Involvement of the corpus callosum is seen in MS and is not seen in NMO. Ring and nodular Gadolinium enhancement of lesions is frequently seen (Fig 1). 1,14 Sometimes, large tumor like lesions can also be seen with MS. These lesions are known as tumefactive MS. These lesions are often atypical for MS and may appear to exert mass effect and also show ring enhancement. They can often be differentiated from CNS tumors by the presence of open ring enhancement directed towards the cortex which is not seen in tumors. They also demonstrate mixed T2-weighted iso and hyper intensity of enhanced regions, and absence of cortical involvement.19 Fig 4 and 5 show two cases of tumefactive MS. Fig 6 shows a case of widespread MS.
In NMSOD, bilateral optic nerve involvement including the chiasm, cervicothoracic spinal involvement and circumventricular organ involvement is seen. The lesions are frequently encountered at the cortico-subcortical junction. Large brainstem lesions may be seen. Spinal cord lesions are longitudinal and may also appear to exert mass effect. Cloud-like and periependymal patterns of gadolinium enhancement are seen in NMOSD.15 Fig 7, 8 and 9 show three separate cases of NMO involving the cerebrum, optic nerves and spinal cord respectively.
The imaging findings of MOG-IgG encephalomyelitis are not very consistently reported in literature due to it being a relatively newly identified disorder. Cerebral lesions are shown in Fig 10. In these patients, bilateral optic nerve involvement sparing the chiasm (Fig 11), conus medullaris and thoracolumbar spinal involvement, basal ganglia, thalamic and infratentorial lesions are commonly seen.15 Fig 12 shows cervicothoracic spinal cord involvement in a case of MOG-IgG encephalomyelitis.
ADEM commonly involves the cortical grey matter, deep white matter with periventricular sparing and thoracic spinal cord. Due to the large size of these lesions (especially spinal cord lesions), mass effect can be observed. All lesions tend to show simultaneous patchy gadolinium enhancement (Fig 13). In some cases, lesions are bilateral and symmetrical. There is rapid resolution of lesions which is not seen in the other demyelinating disorders.3
The imaging findings of Susac’s syndrome are characteristic of the disease. They include periventricular lesions and involvement of the corpus callosum, the latter is not seen in the above-mentioned demyelinating disorders. The callosal lesions are often of CSF density. Another characteristic of these lesions is that they do not enhance with gadolinium. On FLAIR, these lesions are of mixed density (Fig 14).18