The Ne w E n g l a nd Jo u r n a l o f Me d ic i ne

Case Records of the Massachusetts General Hospital

TABLE 1. HEMATOLOGIC LABORATORY VALUES.

Weekly Clinicopathological Exercises
FOUNDED

BY

RICHARD

C.

CABOT

R O B E R T E . S C U L L Y , M. D. , Editor
E U G E N E J . M A R K , M. D. , Associate Editor
W I L L I A M F . M C N E E L Y , M. D. , Associate Editor
S A L L Y H . E B E L I N G , Assistant Editor

VARIABLE

VALUE

Hematocrit (%)
Erythrocyte sedimentation rate (mm/hr)
White-cell count (per mm3)
Differential count (%)
Neutrophils
Lymphocytes
Monocytes
Platelet count (per mm3)

42.4
21
16,700
87
11
2
411,000

Case 26-1998
TABLE 2. BLOOD CHEMICAL VALUES.

PRESENTATION OF CASE

A 15-year-old right-handed girl was admitted to
the hospital because of hemiparesis, slurred speech,
and urinary retention.
The patient had been in excellent health until two
and a half weeks earlier, when she began to have urinary urgency but found it difficult to empty her
bladder. A few days later she felt unsteady and fell
several times. Her handwriting slowed, and she had

Figure 1. Contrast-Enhanced Axial CT Scan Showing a 5-cm
Ring-Enhancing Lesion.
The lesion is centered in the body of the corpus callosum, with
bilateral extension into the centrum semiovale. The rim is
smooth, and there is little surrounding edema.

542 ·

VARIABLE

VALUE

Glucose (mg/dl)*
Sodium (mmol/liter)
Potassium (mmol/liter)
Chloride (mmol/liter)
Carbon dioxide (mmol/liter)

129
141
3.5
106
21

*To convert the value for glucose to millimoles
per liter, multiply by 0.05551.

Figure 2. Axial T2-Weighted MRI Scan Showing Marked Hyperintensity of the Lesion.
There is a small amount of edema with a hyperintense signal,
which is best seen along the left anterior margin of the lesion.

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CASE RECORDS OF TH E MASSACH USET TS GENERA L H OS PITA L

Figure 3. Gadolinium-Enhanced T1-Weighted Axial (Upper Panel) and Coronal (Lower Panel) MRI Scans.
The mass is hypointense. There is relatively smooth enhancement of the rim, with almost no surrounding edema.

difficulty articulating her thoughts. Several days before admission, weakness and numbness developed
in the right arm and leg, accompanied by right facial
droop and slurred speech. On the evening before
admission, she was found sleepwalking for the first
time in her life. She continued to attend school until
the day of admission, when her mother, observing
that the girl needed to use her arms to rise from a
chair, took her to a physician.
A computed tomographic (CT) scan of the brain

(Fig. 1), performed before and after the administration of contrast material, showed a ring-enhancing,
mass-like lesion, 5 cm in diameter, in the corpus callosum, with extension into the centrum semiovale in
each hemisphere and with little surrounding edema.
The patient was referred to this hospital.
The family had a healthy cat. The patient had no
history of antecedent viral infection or vaccination,
foreign travel, neurologic symptoms, altered cognition or mental status, fever, headache, visual disturbance, seizures, weight loss, or tick bite, and she had
no risk factors for sexually transmitted diseases. There
was no family history of brain tumor, multiple sclerosis, or other neurologic disease.
The temperature was 37°C, the pulse was 84, and
the respirations were 20. The blood pressure was
120/70 mm Hg.
The results of a physical examination were normal,
except for obesity.
On neurologic examination, the patient was alert
and fully oriented, with preserved memory and intact speech and comprehension. There was mild
right-central facial paresis, with slight dysarthria. The
medial aspects of the optic-disk margins were
blurred. The right pupil was 4 mm in diameter and
constricted to 2 mm on stimulation with light; the
left pupil was 3.5 mm in diameter and constricted to
1.5 mm. The remaining cranial-nerve functions were
preserved. Strength was graded 4/5 in the right biceps, triceps, and deltoid; 5/5 in the right grip; 4/5
in the right iliopsoas; and was 4¡/5 in the rightknee flexors and extensors and the right plantar flexors and extensors. The strength in the left arm and
left leg was 5/5. Sensitivity to a light touch, pinprick, and heat and cold was normal; stereognosis,
graphesthesia, and coordination were intact. The
deep-tendon reflexes were ++++ in the right arm and
right knee, +++ in the right ankle with sustained clonus, and +++ in the left arm and left leg, with bilateral Babinski signs. The stance was stable, with a
negative result on Romberg’s test. Evaluation of the
gait disclosed slight circumduction, with a minor
limp in the right leg and diminished swing in the
right arm. The patient had difficulty walking on her
toes and performing tandem walking. While making
a quick turn, she staggered.
The urine was normal. The levels of urea nitrogen, creatinine, conjugated and total bilirubin, aspartate aminotransferase, alanine aminotransferase,
lactate dehydrogenase, and alkaline phosphatase were
normal, as was the osmolality. The prothrombin and
partial-thromboplastin times were normal. The results of other laboratory tests are shown in Tables 1
and 2. An electrocardiogram revealed sinus tachycardia at a rate of 113 beats per minute.
Radiographs of the chest were normal. A gadolinium-enhanced magnetic resonance imaging (MRI)
study of the brain (Fig. 2 and 3) disclosed a massVol ume 33 9

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like lesion, 5 cm in diameter, centered in the corpus
callosum, with extension into the centrum semiovale in each hemisphere. The lesion was hyperintense
on T2-weighted images (Fig. 2) and hypointense on
T1-weighted images (Fig. 3), and it had a smooth
enhancing rim. Little edema surrounded the lesion.
A diagnostic procedure was performed.
DIFFERENTIAL DIAGNOSIS

DR. EDWIN L. ZALNERAITIS*: May we review the
radiologic studies?
DR. PAMELA W. SCHAEFER: A contrast-enhanced
CT scan of the head (Fig. 1) shows a ring-enhancing
lesion in the center of the corpus callosum, with bilateral extension into the centrum semiovale. A gadolinium-enhanced MRI study of the brain shows that
the lesion is hyperintense on T2-weighted images (Fig.
2) and hypointense on T1-weighted images (Fig. 3),
with smooth enhancement of its rim and little surrounding edema.
DR. ZALNERAITIS: Problem solving in medicine is
heavily dependent on the recognition of patterns.
To establish the pattern and reach a diagnosis, one
must consider the location, radiologic characteristics,
and pace of the disease process, as well as associated
findings.
Can the single lesion found on the imaging studies in this patient account for her presentation and
all the findings? A lesion in this location could have
disrupted a number of the functions controlled by
the frontal and prefrontal regions of the brain, accounting for several features of the patient’s presentation, including the urinary urgency and sensation of
bladder fullness. Although the supratentorial sites of
urinary urgency and a sensation of bladder fullness
have not been fully established, these symptoms
have been produced by electrical stimulation of the
sensory cortex and by the presence of tumors of the
frontal lobe or lesions of the corpus callosum and adjacent anterior cingulate gyrus.1,2 The patient’s unsteady gait, slow handwriting, and difficulty with articulation of thoughts could be due solely to a
disruption of pyramidal function, as suggested by
her accentuated reflexes and bilateral Babinski signs.
The extent of her disability, however, suggests in addition a dyspraxic state due to a prefrontal disconnection. Prefrontal lesions have also been associated
with proximal weakness and could thus account for
the patient’s need to use her arms when rising from
a chair.3,4
Ruled out by the patient’s history are predisposing factors for her illness. Particularly notable on examination was the absence of fever, alteration in vital
*Director of education and pediatric neurologist, Connecticut Children’s
Medical Center, Hartford; associate professor of pediatrics and neurology
and assistant dean for education, University of Connecticut Medical School,
Farmington.

544 ·

signs, and meningismus. The preservation of cognitive
functions, including most aspects of speech, supports the presence of isolated pyramidal and premotor dysfunction, reflecting a localized process caused
by the single lesion that was identified by imaging.
The patient’s right-sided weakness and slurred speech
are consistent with the presence of pyramidal dysfunction. No elements of the examination as reported in
the case record addressed the specific features of the
dyspraxia. Despite the right-sided numbness, both
primary and cortical sensory perception was unimpaired, a finding consistent with the preservation of
postcentral-gyrus sensory ability. Other parietal functions are not delineated. Since there was no visual
disturbance or other ophthalmologic abnormality
that would explain the blurred disk margins, they
presumably resulted from papilledema due to increased intracranial pressure caused by the mass effect of the lesion, even though the patient had no
headache. Unequal but otherwise intact pupillary
function may be a normal finding or may reflect asymmetric pupillary constriction caused by pressure on
the anterior cingulate region. The patient’s other
motor and reflex changes are consistent with the presence of bilateral but primarily right-sided pyramidal
dysfunction.3
Most of the laboratory test results were normal,
and stress probably accounts for the abnormal results,
including the slightly increased white-cell count,
mild neutrophilia, high platelet count, and slightly
increased glucose level.
The progression of this patient’s disease can be
judged by the development of its manifestations
over a period of two and a half weeks. Although the
lesion undoubtedly preceded the symptoms, its appearance on the unenhanced CT scan — with a rim
of radiodensity greater than that of the surrounding
normal cerebral tissue — reflects a loss of the characteristics of normal brain tissue, a loss common in
rapidly advancing lesions. A recent and symptomatically critical change or the progression of a chronic
condition is much less likely.
What pathologic processes can result in the imaging
findings in this case? The contrast enhancement seen
on both the CT and MRI scans represents a breach
in the blood–brain barrier. This breach may be caused
by a destructive process or by the growth of tissue
that lacks the normal barrier of the central nervous
system, thus allowing contrast material to pass from
the vascular space to adjacent tissue.5,6 The processes
to be considered in this case are those that can evolve
without headache, fever, malaise, or other abnormalities aside from the local effects of the mass-like lesion. Accordingly, we need not consider known causes
of ring-enhancing lesions, such as a thrombosed aneurysm or an infarct or intracerebral hematoma.7
The information in the case record cannot support a precise diagnosis but can be used to generate

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CASE RECORDS OF TH E MASSACH USET TS GENERA L H OS PITA L

a differential diagnosis and then select the most probable diagnosis.
Although ring enhancement is a common finding
in scans of brain abscesses, and although ring abscesses may develop in as short a period as two and a half
weeks, the ring enhancement in this case is thicker
than usual and more characteristic of a neoplasm than
of an abscess. Moreover, an abscess of this size would
be associated with marked edema,7,8 fever, and malaise. Also, predisposing conditions such as cyanotic
congenital heart disease have been reported in as
many as 73 percent of patients with brain abscesses,9
but none of these conditions were present in this case.
Chronic or opportunistic infections, such as tuberculosis or toxoplasmosis, can have this radiographic appearance. When tuberculosis presents as a mass
lesion, however, it is usually more uniformly radiodense, with noticeable edema.10 In addition, this patient’s normal chest film and the absence of fever,
cough, night sweats, or exposure to mycobacteria
make tuberculosis an unlikely diagnosis. Exposure to
a cat can result in toxoplasmosis, even if the cat is
healthy. Lesions due to toxoplasma infection can be
radiographically indistinguishable from the lesion in
this case; surrounding edema is often prominent but
can be minimal, as in this case. Usually there are
multiple lesions. This patient was not immunocompromised and had no additional manifestations of
toxoplasmosis, although such manifestations are not
always present in cases of cerebral infection.11
Demyelinating processes, other than the infectious demyelination found in progressive multifocal
leukoencephalopathy, can present with radiologic
findings similar to those seen in this case. Autoimmune inflammatory demyelination may follow infection with agents such as varicella–zoster virus or
may occur after vaccination. This disorder can result
in a solitary lesion with a mass effect and ring enhancement. With this radiologic appearance, however, the disorder usually has a fulminant course,12
with fever, lethargy, stiffness of the neck, photophobia, malaise, or other manifestations. Therefore, autoimmune inflammatory demyelination is an improbable cause of this patient’s illness.
Demyelination due to leukodystrophy usually appears as a diffuse rather than localized hyperintense
signal on T2-weighted MRI scans. Enhancement is
typically not as prominent as it is in this case, but in
its acute phase leukodystrophy can have a similar radiologic picture.6 Of all the possible explanations for
this patient’s lesion, demyelination due to leukodystrophy is the most likely to be associated with little
surrounding edema, but it probably would not have
as extensive a mass effect as that seen in this case.
Among the leukodystrophies, the most likely to occur
in a teenage patient would be a late-juvenile form of
metachromatic leukodystrophy. Other forms of leukodystrophy occur in an X-linked pattern, such as

adrenoleukodystrophy, or in other age groups, such
as Krabbe’s disease. The patient under discussion had
an isolated lesion, no prior evidence of white-matter
disease such as spasticity or visual impairment, and
no family history of leukodystrophy. Therefore, although metachromatic leukodystrophy is a possible
diagnosis on the basis of the radiologic findings, it
is not a likely cause of the clinical findings.13
In a 15-year-old girl who is otherwise well, a solitary, contrast-enhancing mass lesion in the central
nervous system is most likely a neoplasm. Among
the less common tumors, a lipoma, which is often
located in the corpus callosum, is not a consideration because a lipoma has a lower density on CT
scans and a uniformly high density on T1-weighted
MRI scans. The corpus callosum would be an unusual site for a meningioma, which typically does
not produce an intense signal on either T1-weighted
or T2-weighted MRI scans; its enhancement is typically dense and diffuse. Angiomas most often present
with focal neurologic findings, and complications of
bleeding are the usual cause of acute neurologic
changes. In this case, no changes consistent with the
presence of hemorrhage were noted on the unenhanced CT scan, and the enhancement of an angioma would have been prominent but diffuse. Neither
the clinical course nor the radiologic findings support the diagnosis of angioma.5,6
A primary lymphoma of the central nervous system typically results in diffuse enhancement, and the
signal on T2-weighted MRI scans is usually not as
intense as it is in this case; often there is little surrounding edema. A lymphoma can present with necrosis, a mass effect, and ring enhancement. This
presentation is particularly common with immunoblastic lymphomas, which are not usually located
near the corpus callosum but can occur there.5,11,14
This patient had no immunodeficiency conferring a
predisposition to the development of a lymphoma,
but such a predisposition need not be present. No
clinical features distinguish a lymphoma of the central
nervous system from a glioma.
The location of the lesion in the white matter of
the corpus callosum and the centrum semiovale suggests a glioma, the most common supratentorial
neoplasm seen in this patient’s age group. Oligodendrogliomas can develop rapidly, as did the lesion in
this case, but on T2-weighted MRI scans they produce only a mild signal and slight enhancement with
a fine chicken-wire pattern. A rapidly progressing
glioma with the radiologic characteristics described
in this case would have to be a high-grade astrocytoma or a glioblastoma multiforme. The intense signal
on T2-weighted images, low signal on T1-weighted
images, and ring enhancement best fit the radiologic
appearance of a glioblastoma multiforme, although
the absence of edema around the mass remains puzzling.5,6 The clinical presentation is entirely consistent
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with the presence of an isolated malignant glioma.
Although other possibilities, such as a demyelinating
process, cerebral toxoplasmosis, or a primary central
nervous system lymphoma, cannot be eliminated
without more information, the combined clinical and
epidemiologic features of this case indicate that the
lesion is probably a malignant glioma.
DR. DAVID N. LOUIS: Dr. Ebb, you cared for this
patient. What was your diagnosis?
DR. DAVID H. EBB: Like Dr. Zalneraitis, I favored
the diagnosis of a tumor, most likely a high-grade
glioma such as glioblastoma multiforme or a primary lymphoma.
CLINICAL DIAGNOSIS

Brain tumor: ? high-grade glioma, ? lymphoma.
DR. EDWIN L. ZALNERAITIS’S DIAGNOSIS

Brain tumor, probably malignant glioma.
PATHOLOGICAL DISCUSSION

DR. JEAN-PAUL VONSATTEL: The diagnostic procedure was a biopsy of the left frontal white matter.
Examination of the specimen revealed perivenular
cuffs of lymphocytes and plasma cells (Fig. 4) and
sheets of foamy macrophages containing intracytoplasmic neutral lipids or, in a few instances, myelin
debris (Fig. 5). Also present were reactive mononucleated and multinucleated astrocytes (Fig. 5 and 6)
and a few large protoplasmic glial cells with fragmented chromatin, known as Creutzfeldt cells (Fig.
7 and 8). Myelin was absent, but the axons were relatively preserved (Fig. 9). These histologic features
are consistent with the presence of a reactive demyelinating process, such as multiple sclerosis.
Creutzfeldt cells may be glial cells undergoing abnormal mitosis.15 They are often found in acute
plaques of multiple sclerosis or in astrocytomas.15,16
Creutzfeldt cells are short-lived. Initially their chromatin fragments are located near the center of the
cell (Fig. 7). Later, the fragments move toward the
cell membrane, cytoplasmic vacuoles appear, and
the cell degenerates (Fig. 8).17
In typical cases of multiple sclerosis, numerous
well-outlined gray or tan areas, or plaques, range in
diameter from a few to many centimeters and have
a predilection for the subependymal or periventricular white matter and the subpial white matter of the
brain stem and spinal cord.18 In addition, they tend
to involve the junction of the cortex and subcortex
and may damage the white-matter tracts that traverse the gray matter, as in the globus pallidus. Usually the lesions are of different ages; recent or active
lesions are hypercellular, whereas old lesions are
hypocellular.17 Frequently a vein occupies the center
of a plaque. Perivenular cuffs of lymphocytes and
plasma cells may be prominent in recent or active lesions but are minimal or absent in old lesions.
546 ·

Figure 4. A Vein with a Cuff of Lymphocytes and Plasma Cells
(Hematoxylin and Eosin, ¬300).
The surrounding parenchyma is hypercellular.

Biopsy specimens of diffusely enhancing or ringenhancing lesions are characterized by hypercellularity, the presence of macrophages, and extensive loss
of myelin, occasionally with edema, with or without
cyst formation19; edema is not observed at postmortem examination, however.18 Nonenhancing demyelinating lesions tend to be characterized by fibrillary
astrocytosis, with few macrophages and few or no
inflammatory cells of other types.
The size and distribution of white-matter lesions
can point to the correct diagnosis. In postinfectious
or postvaccination encephalomyelitis, the lesions may
appear large on neuroimaging 20 but small and perivenular on microscopical examination.18
Large white-matter lesions in young children can
be due to Schilder’s disease, a very rare, aggressive
form of multiple sclerosis. In boys, adrenoleukodystrophy, an X-linked recessive disorder of lipids,
can cause extensive damage to the white matter.
Broad demyelination of the centrum semiovale can
be the result of subacute sclerosing panencephalitis
or the acute hemorrhagic leukoencephalitis of Weston Hurst, which is distinguished by hemorrhagic
foci surrounding necrotic venules.21
Multiple sclerosis can be difficult to diagnose by

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CASE RECORDS OF TH E MASSACH USET TS GENERA L H OS PITA L

Figure 7. Hypercellular Parenchyma with a Creutzfeldt Cell
(Arrow) (Trichrome, ¬310).
Fragments of chromatin are visible in the center of the cell.
Myelin is absent.

Figure 5. Mononucleated and Multinucleated Reactive Astrocytes (Small Arrows) and Macrophages with Foamy Cytoplasm
(Large Arrows) (Luxol Fast Blue–Hematoxylin and Eosin, ¬450).
One macrophage (arrowhead) contains intracytoplasmic myelin debris (stained blue). Otherwise, myelin is virtually absent.

Figure 8. Macrophages and a Central Creutzfeldt Cell (Arrow)
with Fragments of Chromatin along the Cell Membrane (Hematoxylin and Eosin, ¬310).

Figure 6. Astrocytes Reactive for Glial Fibrillary Acidic Protein
(Immunoperoxidase Method, ¬345).

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Figure 9. Preserved Axons (Bodian Silver Stain, ¬310).

biopsy. An active demyelinating process may mimic
the histologic appearance of a malignant glioma,
which likewise contains pleomorphic astrocytes, including large Creutzfeldt cells. In 1993, Zagzag et al.19
listed the pathological patterns found in active demyelinating processes that make them difficult to
differentiate from gliomas, including hypercellularity,
pleomorphic astrocytes, mitotic figures, necrosis, and
cystic changes. Histologic features favoring diagnosis
of a reactive process include the presence of foamy
macrophages, reactive astrocytes, and inflammatory
infiltrates; loss of myelin; and absence of vascular
proliferation. Pleomorphic astrocytes, including multinucleated forms, may be conspicuous in active
plaques, especially at the periphery.17 These astrocytes may suggest a neoplasm, but in contrast to neoplastic astrocytes, the reactive cells are not characterized by hyperchromatic nuclei.
In conclusion, an active demyelinating process
such as multiple sclerosis is the most likely pathologic
event when a biopsy specimen from a diffuse or
ring-enhancing white-matter lesion shows perivascular infiltrates of lymphocytes and plasma cells, reactive astrocytes, Creutzfeldt cells, foamy macrophages,
extensive loss of myelin, and relative preservation of
axons.
Dr. Stein saw the patient after the diagnosis was
made.
DR. MARION C. STEIN: The patient initially received corticosteroid therapy, and after three weeks
of treatment, she had recovered enough to return to
school for one day. However, as we tapered the dose,
her condition rapidly deteriorated. Five weeks after
548 ·

the diagnostic biopsy, she was readmitted to the hospital with severe spontaneous extensor spasms and
progressive spastic diplegia that was greater on the
right side than on the left. She had marked emotional
disinhibition, and the dysarthria recurred. Repeated
imaging showed ring-enhancing lesions similar to
those seen previously, except that the enhancement
was somewhat diminished, perhaps because of the
corticosteroid treatment. The right side of the centrum semiovale was somewhat enlarged, as it had been
previously, but the edema in the area of involvement
on the left side was slightly diminished.
The patient’s condition improved clinically only
with intravenous administration of very high doses
of corticosteroid medication (1000 mg of methylprednisolone) and worsened again when the dose
was tapered. An induction regimen of cyclophosphamide was immediately added. After the patient
had received 6 g of cyclophosphamide over a 10-day
period, administered according to the published
regimen for its use in patients with multiple sclerosis, 22 her clinical condition stabilized. She tolerated
tapering of the oral corticosteroid, and her neurologic condition continued to improve. Two months
after treatment, she was able to return to school but
had emotional instability, fatigue, and mild visuospatial defects. Her academic performance was variable, but she was able to maintain her grade level.
A year and a half after the diagnosis, on a very hot
day, she had tingling of the right hand and foot,
which resolved completely by the next day. No further imaging studies were done. The patient has had
no additional episodes, has remained well, and is
college-bound.
DR. LOUIS: The literature suggests that acute
episodes such as those in this patient tend not to
lead to more typical manifestations of multiple sclerosis. Has that been your experience?
DR. STEIN: Yes. I expect that the clinical course of
this patient’s disease will be monophasic. In the past
10 years, we have seen three other cases of aggressive
bilateral, confluent demyelination around the corpus
callosum. There was biopsy confirmation in all the
cases. None of the lesions have recurred. All the patients had only transient responses to corticosteroid
therapy, but their conditions stabilized after they received cyclophosphamide therapy. Only the younger
patients had considerable clinical improvement.
DR. ZALNERAITIS: All the children I have seen
who had monophasic acute episodes of demyelination were lethargic and had other symptoms, unlike
this patient. In your experience, Dr. Stein, do most
of these patients have other symptoms?
DR. STEIN: Lethargy, and even obtundation, fever,
and seizures, may occur in cases of monophasic disseminated myelitis, particularly those that develop
after infection or vaccination. Neither the patient under discussion nor the other, similar patients I have

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CASE RECORDS OF TH E MAS SACH USET TS GENERA L H OS PITA L

treated had any identifiable preceding illness, and the
lesion on the cerebral MRI scan was deep and confluent, not multifocal and disseminated as in postinfectious and postvaccination cases. Although some
of our patients had mutism, aphasia, and diminished
interaction, the clinical and radiologic development
of disease in these patients was still distinct from
that of the patients with postinfectious or postvaccination demyelinating disorders.
DR. SCHAEFER: Demyelinating lesions centered in
the corpus callosum frequently have an imaging pattern different from that of malignant tumors in the
same location. The latter tend to be high-grade tumors with more surrounding edema and a thicker,
more nodular enhancing rim. Therefore, a smooth
rim with little surrounding edema suggests a demyelinating rather than a neoplastic process.
ANATOMICAL DIAGNOSIS

Demyelinating process consistent with the presence of
multiple sclerosis.
ADDENDUM

DR. ZALNERAITIS: Since this clinicopathological
exercise, I have found two additional reports that address the MRI findings in multiple sclerosis. Brück et
al.23 described a case in an adult with clinical findings that were similar and radiologic findings that
were identical to those in the case under discussion.
Takahashi et al.24 reported a case in a child that was
similar to this case clinically but not radiologically;
that patient had recurrences during methylprednisolone therapy but was free of relapses for 18 months
after plasmapheresis.
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©1998, Massachusetts Medical Society.

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