A 28-year-old woman presented with headaches, light-headedness, dizziness, and episodes of emesis. The patient complained of numbness and tingling on the right side of her face. Prior to this, the patient was in her usual state of health. The patient had previously had skin nevi removed that demonstrated "aggressive" histology. She had been taking oral contraceptives for 1.5 years. The patient’s
physical examination was otherwise unremarkable.
A 28-year-old woman presented with headaches,
light-headedness, dizziness, and episodes of emesis. The patient
complained of numbness and tingling on the right side of her face.
Prior to this, the patient was in her usual state of health. The
patient had previously had skin nevi removed that demonstrated
"aggressive" histology. She had been taking oral contraceptives for
1.5 years. The patient's physical examination was otherwise
Cystic multiple sclerosis
A magnetic resonance imaging (MRI) study of the brain was
performed (figures 1 and 2). There were ring lesions in the
posterior right frontal lobe associated with moderated edema
(figure 2). The lesions did not enhance after injection of
gadolinium. The periphery was hyperintense on T2-weighted images
and the central portion of the lesion was isointense on T1-weighted
images and hyperintense on T2-weighted sequences. A few
hyperintense T2 signal abnormalities were present in the centrum
semiovale bilaterally. The differ-ential diagnosis at this point
favored abscess(es), metastatic disease, and less likely an
atypical demyelinating disease.
Given the patient's history of aggressive nevi, a stereotactic
biopsy was performed. The hospital course was uneventful. The
patient was started on steroid therapy.
Multiple sclerosis (MS) is a clinical diagnosis that should
never be made based on imaging results alone. It is best
characterized by episodes of focal neurologic deficits of the
brain, spinal cord, and optic nerves with relapses and remissions.
The progression of the disease is unpredictable with almost certain
disability. Autoimmune-mediated demyelination is favored as a cause
for the disease. There is no cure. Approximately 95% of patients
present between 18 and 50 years of age. MRI with contrast has the
advantage of detecting lesions both in space (location) and time
(acute versus chronic). Lesions appear hypo- to isointense on T1-
weighted and hyperintense on T2-weighted sequences. Occasionally, a
thin peripheral hyperintense T1 signal may be seen attributed to
protein and lipid-laden macrophages and free radicals. Classic
locations for lesions to occur are in the calloseptal interface,
periventricular white matter, corpus callosum, and brachium pontis.
Lesions may also occur in the floor of the fourth ventricle and
periaquaductal gray matter. Some authorities require at least three
lesions of 5 mm or more in size and in the classic locations to
establish the imaging diagnosis.
Histopathologically, there is infiltration of lymphocytes and
plasma cells in a venous perivascular distribution. This produces
the classic periventricular ovoid appearance. There is myelin loss
with relative sparing of axons, nerve cells, and blood vessels. The
cellular inflammatory reaction causes damage to the blood brain
barrier, which allows influx of water and protein, correlating with
contrast enhancement. In the acute setting, this may last for 4 to
Lesions with a similar appearance to MS with regard to imaging
and clinical presentation exist. These are acute disseminating
encephalomyelitis (ADEM), vasculitides, and Lyme disease. ADEM is
distinguished from MS by its single episode of acute onset of fever
and headaches. It rarely relapses. If all lesions enhance, the
likelihood of ADEM increases over MS. Vasculitic lesions tend to be
more peripheral than MS lesions and show infarction in vascular
territories. Lyme disease must be differentiated from MS since the
former is treatable. The clinical presentation of Lyme disease may
also have a waxing and waning course and present with optic
1. Chakrabortty S, et al: Intracerebral
ring-enhancing lesions in a patient with multiple sclerosis: A case
report. Surg Neurol 43:591-594, 1995.
Prepared by Michael S. Goldman, MD and
R. Anthony Lloyd II, MD, Department of Radiology, Division of
Neuroradiology at the University of Maryland Medical School,