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The Brain And Multiple
Sclerosis
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| Clinical Profile |
| Findings |
| Discussion |
| Pathology |
| Variants |
| On MRI |
| Differential Diagnosis |
| Suggested Reading |
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
sulci.
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
type.
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 oligoclonal bands.
Acute MS plaques
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 axis-"Dawson's fingers". Neuroglial infiltration, perivascular mononuclear cells/lymphocytes and oligodendrocytes are also seen. There is a transient break in the blood-brain barrier.
Chronic MS plaques
They usually show gliosis, atrophy and cavitation.
Remyelination may be noted.
Classic-Charcot
Type:
Most common form (discussed above).
Acute-Marburg
Type:
In younger patients. Usually preceded by
fever and has a relentless course. May be the terminal event in classic
MS.
Neuromyelitis Optica-Devic's
disease:
Acute onset of spinal cord and optic
nerve demyelination.
Diffuse Sclerosis-Schilder
Type:
Seen in children. Psychiatric problems
are more common. There is confluent, asymmetric demyelination involving
both cerebral and cerebellar hemispheres and brain stem.
Concentric Sclerosis-Balo
Type:
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 lateral ventricle.
The corpus callosum lesions are best seen on FLAIR sagittal images. Late in the disease thinning of the corpus callosum is commonly seen.
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.
White Matter Ischemia:
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).
Virchow Robin(VR) Spaces:
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.
Lacunar Infarct:
Usually isointense to CSF. May have a hyperintense rim on the Proton, T2W or FLAIR images (gliosis).
Progressive Multifocal Leukoencephalopathy(PML):
Usually the patient is immunocompromised. The lesions affect the
peripheral white matter and tend to be patchy with an asymmetric
distribution.
Other white matter diseases (metabolic and inflammatory
or infective processes) can also mimic MS.
Migraine:
Periventricular hyperintensites are noted which usually mimic white matter ischemia. History is fairly typical.
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