H/O diminished vision on the right side,
headaches, giddiness, gait imbalance, neck pain, paresthesias in all
four limbs and a weak grip since two months.
There are diffuse and focal hyperintense lesions on the T2W
and FLAIR images within the parietal periventricular white matter and
centrum semiovale bilaterally, right periventricular white matter,
medulla, pons and right middle cerebellar peduncle. There is fullness of
the ventricular system and slight prominence of the cerebral cortical
This patient also had lesions in the spinal cord.
Multiple sclerosis is a primary demyelinating disorder
(myelinoclastic disease-myelin destruction whereas there is relative
sparing of the axons).
Patients usually present with weakness, numbness
and tingling of one or more extremities, gait disturbance or visual
impairment or diplopia. They usually have a relapsing/remitting pattern.
Severe spinal cord affliction is more common with the chronic progressive
The exact etiology is unknown. One of the prevailing views is that an
initial viral infection is subsequently followed by an auto-immune
reaction with a resultant attack on the myelin. The MS plaques are usually
found in the white matter of the cerebrum, cerebellum, brain stem, spinal
cord and the optic nerves, chiasm and tracts. CSF may show the presence of
There is destruction of the myelin with axonal sparing.
Usually they occur in a perivenular distribution. This perivascular
demyelination is seen as a finger pointing along the vessel
fingers". Neuroglial infiltration, perivascular
mononuclear cells/lymphocytes and oligodendrocytes are also seen. There is
a transient break in the blood-brain barrier.
They usually show gliosis, atrophy and cavitation.
Remyelination may be noted.
Most common form (discussed above).
In younger patients. Usually preceded by
fever and has a relentless course. May be the terminal event in classic
Acute onset of spinal cord and optic
Seen in children. Psychiatric problems
are more common. There is confluent, asymmetric demyelination involving
both cerebral and cerebellar hemispheres and brain stem.
Has a concentric or lamellar pattern.
Areas of demyelinated and myelinated (? remyelination) white matter
alternate. Is progressive and seen in young people.
MS plaques are seen as discrete foci with well-defined
margins. They are hypointense on the T1W images and hyperintense on the
T2W, Proton and FLAIR images. Occasionally larger lesions may coalesce
to form confluent lesions.
The plaques usually involve the corpus callosum, cerebral
and cerebellar white matter, brain stem, internal capsules and visual
pathways. Subcortical U fibres are commonly involved.
Acute plaques may have a hyperintense rim on the T1W
images or a hypointense rim on the T2W images (? due to free radicals,
proteins or fat-laden macrophages).
The periventricular lesions are commonly located along the
lateral margins of the occipital horns and atria. The perivenular
location gives then an ovoid shape. They are perpendicular to the
The corpus callosum lesions are best seen on FLAIR
sagittal images. Late in the disease thinning of the corpus callosum is
Occasionally the grey matter of the cerebral cortex and
basal ganglia are involved.
The posterior fossa lesions are usually seen to abut the
cisterns or the fourth ventricle or aqueduct.
The area of inflammation reduces in size with time. The
residual plaque is more linear or punctate.
Optic neuritis is commonly seen. The STIR images are
especially sensitive and the nerves appear hyperintense. Enhancement is
best seen using fat saturation images.
Late in the disease cerebral atrophy and ventricular
dilatation is common. Increased iron deposition may be seen in the basal
ganglia (increased hypointensity on the T2W images).
Acute lesions may enhance following Gd contrast
administration. Nodular or ring enhancement is seen. The lesions enhance
for eight to twelve weeks after acute demyelination. Meningeal
enhancement may be seen rarely with acute relapsing MS.
- Following steroids there may be a definite reduction in lesion
enhancement and size.
Usually spares the corpus callosum and the subcortical U fibres.
Cerebral arteritis can result in periventricular hyperintensities and/or
cortical infarcts (Usually have systemic features).
Usually round with an approximate diameter of 1-2 mm. Commonly seen in
the deep white matter on higher sections and basal ganglia. They are
usually isointense to CSF.
Usually isointense to CSF. May have a hyperintense rim on the Proton,
T2W or FLAIR images (gliosis).
Usually the patient is immunocompromised. The lesions affect the
peripheral white matter and tend to be patchy with an asymmetric
Other white matter diseases (metabolic and inflammatory
or infective processes) can also mimic MS.
Periventricular hyperintensites are noted which usually mimic white
matter ischemia. History is fairly typical.
- Simon JH: Neuroimaging of multiple sclerosis: Neuroimaging Clin
North Am 3:229-246, 1993.
- Yetkin FZ, Haughton VM, Papke RA, et al: Multiple Sclerosis:
specificity of MR for diagnosis . Radiology 178:447-451, 1991.
- Hesselink JR: White Matter Disease. In: Edelman RR, Hesselink JR,
Zlatkin MB: Clinical Magnetic Resonance Imaging, W.B. Saunders, Volume
1, pp:851-879, 1996.