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Devic's neuromyelitis optica A clinicopathological study of 8 patients.

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Devic’s Neuromyelitis Optica:
A Clinicopathologcal Study of 8 Patients
Raul N. Mandler, MD,”? Larry E. Davis, MD,* Douglas R. Jeffery, MD,“ and Mario Kornfeld, MDf
We report the clinical, imaging, and laboratory features of 8 patients with Devic’s neuromyelitis optica. All patients
had severe myelopathy and optic neuritis. In no patient was the brain, the brainstem, or the cerebellum affected, even
after several years of disease. Various immunosuppressive treatments failed to benefit the patients, 5 of whom died.
Autopsies of these 5 patients demonstrated a severe necrotizing myelopathy with thickening of blood vessel walls and
no lymphocyte infiltrates. In the appropriate clinical setting, the lack of white matter abnormalities demonstrated by
magnetic resonance imaging of the head facilitates the recognition of Devic’s syndrome during life. Inasmuch as
Devic’s myelopathy is necrotizing, rather than demyelinating, the prognosis of this syndrome is poor.
Mandler RN, Davis LE, Jeffery DR, Kornfeld M. Devic’s neuromyelitis optica:
a clinicopathological study of 8 patients. Ann Neurol 1093;34:162-168
In 1894 Eugine Devic and his student F. Gault reviewed the cases of 16 patients with a syndrome manifested by acute or subacute optic neuropathy with myelopathy, and added one of their patients 11-31. Since
then, Devic’s neuromyelitis optica has been regarded
either as a form of multiple sclerosis (MS) or as a separate neurological syndrome 14-91. Although this dilemma might not be solved as long as the etiology
of MS remains unknown, magnetic resonance imaging
(MRI) could help differentiating neuromyelitis optica
in the strict sense from MS during life. Whereas in
MS multiple areas of abnormal white matter signal are
expected to be found on head MRIs, it is unclear
whether these findings are to be present in patients
with strict Devic’s syndrome. By using gadolinium
diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced MRI, we studied 3 patients recently diagnosed with Devic’s syndrome, one of whom had serial
brain MRIs over a 4-year follow-up. We then reviewed
the clinical, laboratory, and imaging findings of 8 patients with Devic’s syndrome and the pathology in the
5 who died.
When postmortem examinations were done, brain and spinal cords were fixed in 10% formalin for 2 weeks, cut in
0.5-cm-thick serial section; representative sections were embedded in paraffin and cut at 6 to 8 pm. Microscopic sections
were stained with hematoxylin-eosin, Lux01 fast blue-hematoxylin and periodic acid-Schiff (LFB/PAS), and Bodian’s
silver stain. Representative sections were photographed with
a Nikon (Japan) UFX-DX camera. MRI examinations with
and without Gd-DTPA were performed in multiple planes
using T1-, T2-, and intermediate-weighted images on a GE
Signa 1.5-Tmachine (Milwaukee, WI). Central nervous system (CNS) IgG daily synthesis was determined by immunonephelometry [ 111. Cerebrospinal fluid (CSF) and serum
analyses for bands were performed by isoelectric focusing on
polyacrylamide or agarose gels, and stained with Coornassie
blue or silver nitrate, respectively C12).
Eight patients were reviewed based on clinical or pathological
diagnosis, or both, of Devic’s syndrome, Devic’s disease, or
neuromyelitis optica. Inasmuch as the cases of the 8 patients
are similar, pertinent information is displayed in the tables.
Seven patients were hospitalized in Albuquerque, New Mexico, and 1 in Denver, Colorado. Patient 5 has been previously
reported [101.
Illustrative Case Report
A 22-year-old Hispanic American woman (Patient 1) was
healthy until a few months after a miscarriage, when she
developed tingling, numbness, and a truncal sensory level
with progressive ascending paralysis of all extremities and
bladder dysfunction. No abnormalities were present above
the neck. MRIs of the brain with and without Gd-DTPA was
normal on three occasions over a 3-year period. MRIs of the
spinal cord revealed dlffuse enlargement from C5 to TI with
a central area of T2-increased signal and TI-decreased signal
that enhanced with Gd-DTPA (Fig 1).Visual and brainstem
auditory evoked potentials were normal. Somatosensory
evoked potentials revealed abnormal conduction at the cervical level of the spinal cord. CSF examination done during rhe
acute illness disclosed an opening pressure of 150 mm H,O.
The red blood cell count was 0 and the white blood cell
From the Departments of ‘Neurology, ?Anatomy, and $Pathology,
The University of New Mexico School of Medicine and The Vererans Affairs Medical Center, Albuquerque, NM.
Address correspondence to Dr Mandler, Department of Neurology,
The University of New Mexico School of Medicine, Albuquerque,
NM 87131.
Patients and Methods
Received Dec 15, 1992, and in revised form Feb 10 and Mar 10,
1993. Accepted for publication Mar 10, 1993.
162 Copyright 0 1093 by the American Neurological Association
Fig I Patient 1. Abnormal-appearing magnetic ruonance image of the cervical and thoracic regions of the spinal cord. This
TI -weighted image (TR GOOITE 20) with gadolinium dzethylenetriaminepentaucetic acid (Gd-DTPA) was obtained with a
1S-T magnet and spine coils. An area of cavitation in the center of the cervical region extends from G3 t o lower cervical leveh,
and is surrounded by areas of Gd-DTPA enhancement that
project into the upper thoracic levels. The cord also shows dzxuse
swelling, especially at C.1-4.
~
(WBC) count was 35 mm3. Total protein concentration was
59 w i d 1 (normal < 45 mgidl). No oligoclonal bands were
detected. The CNS IgG daily synthesis and CSF IgG index
were both normal (0 mgiday and 0.42 and 0.42 mgidl, respectively). Myelin basic protein was normal at 0.7 ng/ml
(normal < 4 ngiml). The CSF albumin level was increased
at 61 mgidl (normal, 8.4-34.2 mgidl) with a serumiCSF
albumin ratio decreased at 65 (normal, 130-370); the IgGalbumin ratio was normal at 14.4 (normal, 9.0-25.0) [13J
The patient received 1gm/day of intravenous methylprednisolone. Symptoms transiently improved but 9 months later,
acute complete blindness of the right eye did not improve in
spite of intravenous methylprednisolone therapy. Cyclophosphamide provoked marked leukopenia and was discontinued.
Subsequently, the patient was maintained on oral prednisone (60 mgiday) with a slow decrease in dose over months.
When attempts to discontinue the prednisone were made,
upper extremity weakness, lower extremity tingling, neck
pain, and visual scoroma of the left eye would relapse. Her
terminal event occurred 4 years after disease onset, when
acute, fulminant ventilatory failure occurred. An MRI of the
cervical region revealed a new area of decreased signal at
the C2 segment. The patient died a few weeks later due to
pulmonary embolism. An autopsy was performed.
Results
Clinical Features
The common denominator of all 8 patients was strict
neuromyelitis optica of poor prognosis in the absence
of CNS disease elsewhere (Table 1). Patient 2 had
concomitant Alzheimer’s disease. In Patient 8 the spinal cord involvement extended to the cervicomedullary junction. In the rest, no brain, brainstem, or cerebellar findings were detected. Follow-up ranged from
1 to 4 years, with a mean of 2.6 years. All patients
were women. Ages at the time of diagnosis ranged
from 22 to 7 3 years, with a mean of 47 years. Four
patients were Anglo-Saxon Americans; 3, Hispanic
Americans; and 1, African American. The disease
started as a myelopathy in 4 patients, an optic neuropathy in only 1, and simultaneous myelopathy and optic
neuropathy in the other 3. Four patients suffered relapses whereas 1 had remitted and improved (Patient
5). Five patients died and underwent postmortem examinations. These patients died between 1 and 4 years
after the initial presentation (mean, 2 years). The other
2 patients had severe neurological sequelae with blindness, paraplegia, and incontinence of urine and stools.
A variety of treatment modalities, including steroids,
corticotropin (ACTH), cyclophosphamide, plasmapheresis, and lymphocytaplasmapheresis were used. When
attempts were made to withdraw steroids, Patients 1
and 4 suffered relapses. Cyclophosphamide produced
severe side effects in Patients 1 and 8. Patient 5 was
pregnant when she developed clinical disease and was
treated with lymphocytaplasmapheresis. She sustained
a complete recovery that lasted for at least 4 years.
Plasmapheresis in Patient 7 did not change the disease
course.
Imaging and Cerebrospinal Fluid Stadies
MRI studies were done in patients examined after
1987 (Patients 1, 7 , and 8 ) (Table 2). In all 3, brain
MRI was normal, even when repeated after years of
follow-up. Spinal cord MRIs, however, showed abnormalities such as enlargement and cavitation in cervical
and upper thoracic areas. Computed tomography (CT)
of the head with contrast media was done in 5 patients
and in all the results were normal, except for cortical
atrophy in the patient with Alzheimer’s disease (Patient
2). Five patients had myelographic examinations. Three
of them showed enlargement of the cervical and upper
thoracic regions of the spinal cord. Two of the myelograms were normal.
CSF studies were done in all patients (see Table 2).
Opening pressures were all within normal limits. Leukocyte (WBC) counts ranged from 0 to 182/mm3,with
a mean of 59 mmj (normal < l/mm3), Total protein
concentration ranged from 39 to 176 mg/dl, with a
mean of 93 mg/dI (normal, 15-45 mg/dI). IgG ranged
from 4.5 to 16.0 mg/dl, with a mean of 9.4 mg/dl
(normal < 4.5 mg/dl). CNS daily 1gG synthesis was
measured in Patients 1 and 7 , with normal results. The
CSF albumin level was abnormal in the 3 patients studied (61, 65, and 63 mg/dl; normal, 8-34 mg/dl). OliMandler et al: Devic’s Neuromyelitis Optica
163
Table I . Clinical Features in Devic’s Neuromyelitis Optica
~~~~~~~
Pauent Age
Ethnic
Fust
No *
(yr) Sex Background Syndrome
22
F
Myelopathy
~~~~
Optic
Neuroparhyl
Optic
Myelopathy
Neuropathy Internal
Course
Years of
Other CNS
Follow-up Involvement
Pregnancy
Acute
4
None
Miscarriage Faral
lnrravenous
methylprednisolone,
predmsone,
steroid-dependent,
cyclophospbnidc
not tolerated
Acute
1
Dementia,
Alzheimcr
No
Fatal
Antibioucs,
pncnytoin
3
None
No
Fatal
Prednmne,
methenamme
mandelatc
(Mandehine)
Nu
Peripheral
neumpathy
Fatal
Prcdnisone
Simulraneous Acute
4
remrtting
None
Pregnant
(6 mo)
Improved
Lymphocytaplasmapheresis,
pheresis-dependent
Hispanic
Myelopathy
American
Acute.
relapsing;
C5-T1,
T7, c 2
Acute.
righi
18 mo
4 mo
Outcome
relapsing
Treatment
73
F
Hispanic
Optic
American
neuropathy
Acute,
Acute,
pmgresive;
left
52
F
AngloMyelopathy
Saxon
American
Acute,
Acute,
progressive;
left
T8-C3
11 mo
Acute
rekpsmg
50
F
AngloMyelopathy
Saxon
American
Acute,
Acute,
left
progressive;
32 IW
Acute
2
relapsing
26
F
Angb
Optic
Acute,
Saxon
neumpathy,
remitting,
American
myclopathy
T5
49
F
Hispanic
Optic
American
nempdthy.
myelopathy
Acute,
Acute,
progressive;
left
T5
Simultaneous Acute
2
None
No
Severe visual Prednisone,
and
conicotropin
ambulatory
deficits
58
F
AngloOptic
Acure,
Acute,
Saxon
neuropathy,
progressive,
left
American
myelopathy
C3-4
Simulraneous Acute
2
None
No
Severe visual Plasmapheresis
and
ambulatory
deficits
30
F
African
Optic
Acute,
Acute,
American
neuropathy,
progressive,
left
myelopathy
C1-5
24 mo
Cemcomedullary
junction
No
Fad
C5
T3-C5
Acute,
left
Acute
3
relapsing
Intravenous
methylprednisolone,
cyclophospharmde
(Cytoxan),
conicotropin
“Case 8 1s from Denver. CO All others are from New Mexico
goclonal bands were not detected in 6 of 7 patients, in
spite of multiple CSF studies done in some patients
over months and years. In Patient 5 no oligoclonal
bands were detected initially but they appeared 5
weeks after the onset of the disease. This patient’s CSF
was not reexamined a third time.
nerves, did not display abnormal vessels. The optic
nerves and chiasma were demyelinated in all subjects,
with gliosis and cavitation seen in 2 of them. Remarkably, no demyelinated or necrotic lesions were detected in the brain, brainstem, or cerebellum by using
LFB/PAS stains.
Pathological Featares
Discussion
This clinicopathological study demonstrates that Devic’s neuromyelitis optica sensu strictu occurs in AngloSaxon Americans, Hispanic Americans, and African
Americans. The clinical, imaging, CSF, and pathological features are sufficiently distinctive from those usually observed in MS 1141. A major difference between
these 8 patients with Devic’s syndrome and MS patients is the absence of brainstem, cerebellar, and cognitive findings in the former group, even after several
years of follow-up in some cases.
The important, negative imaging finding was the absence of white matter abnormalities on head MRIs. On
the contrary, multiple white matter abnormalities are
usually seen in head MRIs of MS patients. Furthermore, in MS those abnormal areas are sometimes
asymptomatic, suggesting that the disease continues its
course in spite of apparent clinical remission ClS]. The
other important MRI finding that correlated with the
The pathology was similar in all 5 patients (Table 3,
Fig 2). The spinal cord was severely affected throughout most of its length. Microscopically, the pathological
hallmark was cavitation and necrosis of both gray and
white matter. Macrophages were abundant in necrotic
areas. Small spinal cord vessels were prominent in necrotic and perinecrotic areas. Remarkably, vessel walls
were enlarged and hyalinized, with scarce nuclei. No
mononuclear cell infiltrates, except for macrophages,
were detected around these abnormal vessels. In some
instances, distinction between the arterial and venous
nature of these vessels could not be established. Some
Fessels had a narrow lumen due to wall thickening,
without thrombi. In many of the vessels endothelial
nuclei could not be seen. Except for very few lymphocytes around some meningeal vessels, most parenchymal vessels had no lymphocyte or plasma cell infiltrates. The remainder of the CNS, including the optic
164 Annals of Neurology Vol 34 NO 2 August 1993
Table 2. Imaging and Cerebrospinal Fluid Features in Dwic? Syndrome
Cerebrospinal Fluid
11188
1988, nl
1989, nl
1990, nl
1988, nl
1977
CT showed
CoKiCd atrophy
No white marrer
ahnormahties
1988 MRI. enlarged,
cawrated spinal
cord ar C5-Tl
1990 hlRI, enlarged,
cavltatrd spinal
cord at c2
Enlarged cervical
cord b)
myelographv
Not done
35
59
7.8
61
0
None
0
57
4.5
Not done
Not done
None
1972
Nor done
NI mvclography
IS
176
l3.U
Not donc
Nu1 done
NOW
1976
Nor done
E n h g e d lower
cewicd
cord by
mgelography
2’
I49
12.0
TCot done
Not donc
None
1981
NI LT
Nor dune
182
58
Ih0
Nor done
Kot done
None mindly
Appeared 1 mu
after diagnosis
1982
Not
NI myrlugmphy
198;
NI MRI
NI CT
I YYO
Nl and nl
MRI
MRI
MRI
CT
=
~ I I C
NI MRI
N1 CT
Enlarged
ad
58
39
7.0
Not done
Not done
None
97
114
5.9
65
0
Kone
40
87
ra*rcated cervaal
cord hv MRI
Enlarged cerwcoj
curd by
myelogmphy
Enlarged and
cavirared cervical
cord b) hlR1
normal
syndrome was the swelling and cavitation of the spinal
cord flb}.
Our study also demonstrated that CSF abnormalities
differ from those usually found in MS. The high CSF
albumin level with low serum/CSF albumin ratios suggested a permeability defect in the blood-brain barrier
[13]. With the exception of the 1 patient in whom
transient oligoclonal bands were found, CSF lacked oligoclonal bands. These results agree with a recent study
that found abnormal permeability in the blood-brain
barrier in 2 patients with Devic’s syndrome C171. Interestingly, these authors also found that immunosuppressive treatment produced severe side effects in 1 of
their 2 patients. Moreover, they reported that oligoclonal bands transiently appeared and then disappeared in
1 of their 2 patients. Their other patient never had
CSF oligoclonal bands. MS patients, on the other hand,
usually have increased CNS IgG daily synthesis and
oligoclond bands, as a reflection of intrathecal IgG synthesis by restricted clones of plasma cells located
around venules in the proximity of inflammatory and
demyelinated areas.
The availability of postmortem CNS tissue in 5 patients allowed for pathological correlation with the clinical and imaging findings. In spite of the fact that the
ages of those patients ranged from 26 to 74 years at
the time of death, and that the disease lasted from
1 to 4 years, the pathological findings were virtually
identical. Optic nerves and chiasma were markedly demyelinared or cavitated. All spinal cords were extensively necrotic with cavitary lesions at various levels.
In contrast with acute MS lesions, we found few if
any areas of lymphocytic infiltration. The absence of
perivascular lymphocyte infiltration possibly relates to
the absence of intrathecal IgG synthesis and the lack
of CSF oligoclonal bands.
The lack of lesions elsewhere in the CNS, even after
3 and 4 years of disease (Patients 3 and 1, respectively)
is in marked contrast with the finding of disseminated
sclerotic plaques in MS. Furthermore, the presence of
blood vessel wall abnormalities in the spinal cord but
not in the optic nerves or other CNS areas was most
striking. Similar vessel abnormalities had been described in 2 patients 118, 191 whose syndromes were
closely related to the subacute necrotic myelitis of Marie, Foix, and Alajouanine [20]. Similar pathological
findings were later reported from another patient 12 11
and were also described in patients with lupus and tuberculosis. In all 8 patients, the prognosis was poor
and a variety of immunosuppressive agents yielded no
lasting benefits, except for Patient 5.
We believe that Devic’s syndrome in the strict sense
Mandler et al: Devic’s Neuromyelitis Optica
165
Table 3. Patholorn in Deuic’s Neuromyelitis Optic,
Patient
No.
Spinal Cord
Cavitation and necrosis
from C2-Ll
involving gray and
white matter
Enlarged walls of spinal
cord vessels
Cavitation and necrosis
from Cj-L1
involving gray and
white matter
Enlarged walls of spinal
cord vessels
Optic Nerves
Brain
Brainstem
Cerebellum
Demyelination of the
right one
N o lesions
No lesions
No lesions
Demyelination of the
left one with
macrophages and
astrocytes, without
cavitation
No white matter
lesions
Cortical sulci atrophy
with neuronal cell
body loss,
granulovacuolar
degeneration, and
senile plaque
No lesions
Senile plaques
Granulovdcuolar
degeneration
Senile plaques
No lesions
No lesions
No lesions
No lesions
No lesions
No lesions
Cervicomedullary
involvement
with necrosis
and cavitation
No lesions
Cavitation and necrosis Demyelination of the
left one and chiasma
from C5-T 11
with astrocytosis,
involving gray and
reactive gliosis, and
white matter
microcavitation
Enlarged walls of spinal
cord vessels
Cavitation and necrosis Demyelination of the
left one and chiasma
from C6-l.3
with astrocytosis,
involving gray and
reactive gliosis, and
white matter
microcavitation
Enlarged walls of spinal
cord vessels
Patient alive
Patient alive
Patient alive
Cavitation and necrosis Demyelination of the
left one with
from Cl-T5
astrocycosis, reactive
involving gray and
gliosis, and
white matter
microcavitation
Enlarged walls of spinal
cord vessels
is a distinctive clinicopathological entity, different from
MS. Our paper reports the largest original study of
Devic’s neuromyelitis optica based on clinical, laboratory, MRI, and pathological information to substantiate
OUT hypothesis. Inasmuch as the etiology of MS and
Devic’s neuromyelitis optica is not known, the distinction between thcse conditions needs to be established
on clinicopathological grounds at the present time.
More studies will be necessary to find the etiology of
Devic’s. In any case, the necrotizing nature of the myelopathy with involvement of large areas of the spinal
cord gray matter is a hallmark in Devic’s syndrome but
not in MS.
Pathologically, the contrast between MS and Devic’s
neuromyelitis optica is striking. In the former, scattered demarcated lesions (plaques) that vary greatly in
size, shape, and age are found in white matter areas
of the brain, brainstem, cerebellum, optic nerves, and
spinal cord 122). O n MRI, those plaques most likely
correspond with multiple areas of increased atten-
166 Annals of Neurology Vol 34 No 2 August 1993
uation coefficient in T2-weighted images. When lesions are acute, they enhance with Gd-DTPA. Often,
plaques are adjacent to the ventricular system, especially at the lateral angles of the lateral ventricles. O n
the contrary, the necrotizing nature of the myelopathy
in Devic’s syndrome is most distinctive, as seen in our
pathological studies of 5 patients and others ClS, 19,
21). Cavitation and necrosis of large areas of both gray
and white matter always OCCLX. Furthermore, none
of our 5 patients showed evidence for white matter
plaques in the brain, brainstem, or cerebellum, areas
that are commonly affected in MS. The absence of
these plaques explains the normal appearance of head
MRIs in our patients, even after many years of disease.
Microscopically, the hallmark of the necrotic lesion
is the thickening of the blood vessel. It is possible that
acute edema within a nonstretching pial membrane
might be pathogenically important in the development
of spinal cord necrosis, but more studies are needed
in this respect. The lack of lymphocytic infiltration at
2. Inuging: Normal-appearing brain MRI; enlargement and cavitation on spinal cord MRI.
3. Cwebrupimz,?juid: Decreased serumlCSF albumin
ratio with normal CNS daily IgG synthesis and usually an absence of oligoclonal bands.
4. Puthology: Spinal cord necrosis and cavitation with
thickened vessel walls and absence of inflammatory
infiltrates; demyelination of optic nerves with or
without cavitation; no demyelinating lesions in the
brain, brainstem, or cerebellum.
Future prospective studies will have to take into consideration the spinal cord vessel ahnormality as putatively relevant in the development of Devic's necrotizing myelopathy. The involvement of the spinal cord
and optic nerve with preservation of other CNS structures remains puzzling. Effective therapy remains to be
established.
This work was supported in part by National Institutes of Health
grants R2') NS2'698. BRSG SO' RR 05583-24, and MBRS SO6
GMOX139 (to R. N. M.) and the Research Service, Deparrment of
Veterans Affairs (to L. E . D.).
We thank D r R. Murray (Rocky Mountain Multiple Sclerosis Center,
Inglewood, CX>) for having shared with us his case and D r Askiel
Ijruno for revising the manuscript.
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Fig 2. hlicroscopis pathology of the spinal cord. The sections
were stuined with hemto.yylin-eosin. Representative secti0n.r Patient I ) are JiJplayed. Findiings in aN 5 putients were t'irtua&
identic-a/.iA) Large areas of cmitaiion and nesrosir affect both
gray and white matter ut the C4-5 level. i x 40 bejore 52%
redui-tion.! Other segments d t the rertical, tharacis, and bmbar
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sma" and medium-size clesseLi with enlarged thick uuIhqb u no
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neuromyelitis, patients, optical, stud, devid, clinicopathologic
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