Myelopathy of unknown etiology. A clinical follow-up and MRI study of 57 cases


Martí-Fàbregas, J.; Martínez, J.M.; Illa, I.; Escartín, A.

Acta Neurologica Scandinavica 80(5): 455-460

1989


After a careful differential diagnosis of 264 consecutive cases of spinal cord syndrome seen over a period of 10 years, no diagnosis was reached in 72 patients. Of these cases, known as myelopathy of unknown etiology (MUE), 57 were followed-up for a mean of 2.33 years, 50 being chronic cases and 7 acute cases. Diagnosis was reached in 29 (58%) of the 50 chronic cases, the remaining 21 (42%) still being of unknown etiology. The most frequent diagnosis was either definite or probable multiple sclerosis (MS). Magnetic resonance imaging (MRI) was of great value in detecting asymptomatic brain lesions. We conclude that after a long clinical follow-up and the use of MRI we were able to diagnose more than half the previously MUE patients.

Acta
Neurol.
Scand., 1989:80:455-460
Key
words:
multiple
sclerosis;
magnetic
resonance
imaging;
spinal
cord
diseases;
paraplegia.
Myelopathy
of
unknown
etiology
A
clinical
follow-up
and
MRI
study
of
57
cases
J.
Marti-Fabregas,
J.
M.
Martinez,
I.
Illa,
A.
Escartin
Department
of
Neurology,
Hospital
de
la
Santa
Creu
i
Sant
Pau,
Barcelona,
Spain
ABSTRACT
-
After
a
careful
differential
diagnosis
of
264
consecutive
cases
of
spinal
cord
syndrome
seen
over
a
period
of
10
years,
no
diagnosis
was
reached
in
72
patients.
Of
these
cases,
known
as
myelopathy
of
unknown
etiology
(MUE),
57
were
followed-up
for
a
mean
of
2.33
years,
50
being
chronic
cases
and
7
acute
cases.
Diagnosis
was
reached
in
29
(58%)
of
the
50
chronic
cases,
the
remaining
21
(42%)
still
being
of
unknown
etiology.
The
most
frequent
diagnosis
was
either
definite
or
probable
multiple
sclerosis
(MS).
Magnetic
resonance
imaging
(MRI)
was
of
great
value
in
detecting
asymptomatic
brain
lesions.
We
conclude
that
after
a
long
clinical
follow-up
and
the
use
of
MRI
we
were
able
to
diagnose
more
than
half
the
previously
MUE
patients.
Accepted
for
publication
May
2,
1989
Spinal
cord
syndromes
may
be
caused
by
many
etiologies
(1).
There
is
however
a
large
group,
the
myelopathies
of
unknown
etiology
(MUE),
in
whom
the
etiology
remains
unknown
after
differ-
ential
diagnosis
(2,
3).
Multiple
sclerosis
(MS)
may
be
diagnosed
in
some
MUE
patients
after
a
long-term
follow-up.
MUE
have
been
poorly
studied
and
only
one
necropsic
series
has
been
published
to
date
(3).
Information
regarding
the
clinical
course
of
the
disease
and
laboratory
and
radiologic
data
are
scarce.
We
report
here
the
analysis
of
57
cases
of
MUE
seen
over
10
years,
and
describe
the
clinical
characteristics,
the
number
with
MS
and
the
im-
portance
of
MRI
in
detecting
asymptomatic
brain
lesions
in
some
of
these
patients.
Material
and
methods
We
studied
264
consecutive
cases
of
myelopathy
in
adults
seen
in
the
Department
of
Neurology
in
the
Hospital
de
Sant
Pau
between
1978
and
1987.
All
had
clinical
spinal
cord
syndromes
defined
as
para-,
tetra-
or
hemiparesis,
varying
degrees
of
sensory
loss
and
sphincter
dysfunction
without
symptoms
or
signs
of
central
nervous
system
abnormality
above
the
cervical
spinal
cord
level.
Compressive
and
traumatic
lesions
were
exclud-
ed.
Etiology
was
determined
in
192
patients
(Table
1);
etiology
was
therefore
unknown
for
72
patients
(27%).
Total
number
of
patients
includ-
ed
in
the
study
was
57,
as
15
of
the
72
were
excluded
because
of
inappropriate
follow-up
or
incomplete
study.
The
mean
follow-up
was
28.0
months
(range
6
to
93
months).
Myelography
and/or
MRI
was
carried
out
to
exclude
compressive
lesions
in
all
but
2
cases
(which
had
a
definite
MS).
Myelog-
raphy
was
performed
in
41
patients
and
MRI
in
37
(37
cerebral
and
34
spinal
MRI).
Serologic
studies
including
13
12
and
folate
levels,
serum
electrophoresis,
ANA
determina-
tions,
CSF
examination
(including
total
and
dif-
ferential
cell
count,
glycorrhachia,
proteinorrha-
456
MARTI-FABREGAS
ET
AL
Table
1
Final
diagnosis
obtained
in
264
patients
with
myelopathy
Multiple
sclerosis
55
Spondylosis
and
protruded
intervertebral
discs
50
Vascular
disease
(ischemia,
hemorrhage,
vascular
malformation)
18
Syringomyelia
10
Poliomyelitis
9
Syphilis
5
Other
infections*
4
Cirrhosis,
portocaval
shunt
5
Subacute
combined
degeneration
of
the
spinal
cord
3
Hereditary
spastic
paraplegia
7
Vertebral
disease
or
spinal
canal
compromise"
21
Others***
5
Myelopathies
of
unknown
etiology
72
Total
264
*Includes
Pott's
disease,
AIDS,
neurobrucellosis
and
post-
meningitis
myelopathy;
**includes
spinal
canal
stenosis
at
any
level,
scoliosis,
vertebral
flattening,
craniovertebral
junction
anomalies
and
Paget's
disease;
***includes
clioquinol
myelo-
pathy,
leukodystrophy
and
radiation
myelopathy.
chia
and
protein
electrophoresis)
and
VDRL
were
normal
in
all
patients.
In
20
cases
visual
and/or
somatesthetic
evoked
potentials
were
per-
formed.
Microbiological
studies
were
performed
where
appropriate.
EMG
was
also
done
to
ex-
clude
motor
neuron
disease
or
radiculopathy
in
10
,
number
of
cases
10
20
JO
40
age
iyeers)
Fig.
I.
Classification
of
MUE
by
sex
and
age
at
time
of
consultation.
Table
2
Pathologic
antecedents
without
etiologic
relation
with
the
dis-
ease
in
patients
with
MUE
Trauma
1
Contraceptives
2
Alcohol
Familial
antecedent
of
myelopathy,
MS
or
gait
disturbance
5
Tuberculosis
1
Liver
disease
3
Vertebral
disease
3
Electric
injury
1
Bell's
facial
palsy
2
Idiopathic
thrombocytopenia
purpura
2
Incomplete
vaccination
1
Polyarthritis
1
Encephalomyelitis
1
some
patients.
Spinal
cord
angiography
was
per-
formed
in
only
3
cases.
As
MRI
studies
began
in
our
Department
in
1985,
some
patients
with
MUE
were
studied
late
in
their
follow-up,
and
others
at
the
beginning.
MRI
strongly
suggested
MS
if
there
was
more
than
one
lesion
of
high
intensity
on
T2-weighted
sequences
and
located
predominantly
in
the
white
matter
(periventricu-
lar
or
subcortical).
T2-weighted
high
intensity
lesions
on
spinal
cord
were
only
taken
into
ac-
count
for
MS
when
associated
to
brain
images.
Clinical
diagnosis
of
MS
was
determined
by
the
criteria
of
Poser
et
al
(4).
Results
The
study
group
comprised
29
men
and
28
wom-
en.
Mean
age
at
the
onset
of
symptoms
was
37.9
years
(35.8
for
women
and
39.9
for
men),
while
the
mean
consulting
age
was
43.3
years
(41.2
for
women
and
45.3
for
men).
Approximately
70%
of
cases
were
younger
than
50
years
(Fig.
1).
Pathologic
antecedents
were
considered
out-
standing
in
26
cases,
but
in
no
case
were
of
etiologic
importance
(Table
2).
The
first
clinical
manifestation
of
disease
was
reported
to
be
sensory
disturbance
in
20
cases,
weakness
in
12,
pain
in
8,
sphincter
disturbances
in
7
and
a
combination
of
the
above
in
10
pa-
tients
(Table
3).
The
actual
reasons
for
consult-
ing
physician
were
motor
disturbances
(53/57),
followed
by
sensory
problems
(40/57),
sphincter
0
70
80
60
MYELOPATHY
AND
MRI
457
Table
3
Clinical
symptoms
in
patients
with
MUE
Initial
symptom
Consulting
symptom
Sensory
disturbance
hypoesthesia
dysesthesia
paresthesia
20
(35%)
40
(70's)
Lhermitte's
sign
Motor
disturbance
weakness
gait
disturbance
12
(21%)
53
(93%)
Pain
radicular
vertebral
other
8
(14%)
21
(37%)
Sphincter
disturbance
urgency
and/or
incontinence
(vesical
and/or
rectal)
7
(12%)
36
(63%)
Combinations
of
the
above
10
(18%)
Visual
blurring
during
seconds
1
Limb
atrophy
4
Cramps
6
Fever
in
the
previous
days
3
Fasciculations
2
Toxic
syndrome
1
Hypoacusis
1
Dysarthria
1
Tremor
1
Dizziness
1
disturbance
(36/57)
and
pain
(21/57).
Other
symptoms
of
less
importance
are
also
expressed
in
Table
3.
The
neurologic
examination
disclosed
weak-
ness
in
42/57
(lower
limbs
only
in
26,
upper
and
lower
limbs
in
15
and
only
1
patient
had
upper
limb
weakness).
In
71%
the
paresis
was
asym-
metrical.
Sensory
disturbances
of
the
exterocep-
tive
type
were
found
in
36
patients,
with
a
dorsal
level
in
24
patients,
cervical
in
8,
while
lumbar
level
was
found
only
in
4
cases.
Sensory
disturb-
ances
of
the
proprioceptive
type
were
elicited
in
26
cases.
Hyperreflexia
was
found
in
37/57
pa-
tients
and
absent
or
decreased
reflexes
in
12
cases.
A
Babinski
sign
was
obtained
in
45
cases
(9
unilateral
and
36
bilateral),
while
in
12
pa-
tients
the
plantar
reflex
was
flexor.
The
muscle
tone
findings
were
available
in
only
35
patients,
26
of
whom
were
considered
spastic
(Table
4).
Table
4
Clinical
signs
obtained
by
neurologic
examination
Motor
system
Paresis/paralysis
42
(74
%)
Upper
limbs
15
(26%)
one
limb
10
both
limbs
5
lower
limbs
41
(72%)
one
limb
13
both
limbs
28
upper
limbs
only
1
No
paresis/paralysis
15
(26%)
Asymmetry
30
(71%)
Sensory
findings
Exteroceptive:
hypesthesia
level
dorsal
36
24
(63%)
cervical
8
lumbar
4
asymmetry
23
(40%)
Proprioceptive:
hypesthesia
26
(46%)
Plantar
reflex
Flexor
or
absent
12(21%)
Extensor
(unilateral)
9
(16%)
Extensor
(bilateral)
36
(63%)
Muscle-stretch
reflexes
pathologically
increased
37
(65%)
decreased
or
any
one
absent
12
(21%)
normal
8
(14%)
asymmetry
39
(68%)
Muscle
tone
(of
35
patients)
spastic
26
(74%)
normal
or
hypotonicity
9
(26%)
Visual
evoked
potentials
were
carried
out
in
8
patients,
and
were
abnormal
in
5.
Eleven
patients
had
visual
and
somatesthetic
evoked
potentials,
abnormal
in
4
cases.
Finally,
in
1
case
somat-
esthetic
evoked
potentials
alone
were
performed
with
pathologic
results.
CSF
analysis
were
performed
in
38
patients
and
was
abnormal
in
13.
Oligoclonal
bands
were
observed
in
4
patients,
hyperproteinorrhachia
with
pleocytosis
in
5
and
hyperproteinorrhachia
alone
in
4.
Myelography
was
carried
out
in
41
patients
and
was
normal
in
all
cases.
MRI
was
done
in
37
patients
(Tables
5,
6)
and
was
considered
normal
in
19
patients
(51%)
and
pathologic
in
18
(49%).
In
14
of
the
pathologic
cases
the
images
were
suggestive
of
MS
and
a
simple
image
was
observed
in
the
spinal
cord
in
4
458
MARTI-FABREGAS
ET
AL
Table
5
MRI
findings
depending
on
the
clinical
diagnosis
made
before
performing
the
test
MRI
MRI MRI
with
an
suggestive
normal
spinal
cord
of
MS
image
alone
Definite MS
6
0
0
Probable
MS
4
4
0
MUE
4
14
1
Acute
myelopathy
0
1
3
Total
14
19
4
cases.
Cerebral
and
spinal
studies
were
made
in
all
except
3
patients
from
the
group
suggestive
of
MS,
in
whom
cerebral
MRI
study
alone
was
performed.
1.
Spinal
cord
images
alone
with
a
normal
cerebral
MRI
were
found
in
the
site
of
the
clin-
ical
symptoms
in
3
cases
of
acute
myelopathy
and
only
in
1
case
of
chronic
progressive
myelo-
pathy.
To
date,
all
4
cases
remain
clinically
sta-
ble.
2.
Cerebral
MRI
suggestive
of
MS
was
found
in
14
cases.
In
6,
MRI
only
confirmed
the
previ-
ous
clinical
diagnosis
of
definite
MS
made
on
follow-up.
Four
cases
classified
as
probable
MS
by
clinical
diagnosis
made
on
follow-up
were
reclassified
as
definite
MS
following
MRI.
Four
other
patients
with
diagnosis
of
MUE
could
be
classified
as
probable
MS
due
to
pathologic
MRI.
One
of
these
patients
had
definite
MS
after
clinical
follow-up,
while
the
other
3
are
still
probable
MS
after
follow-up
of
6,
13
and
23
months
respectively.
A
spinal
MRI
study
was
performed
in
11
of
the
14
patients
of
this
group.
Table
6
Influence
of
MRI
findings
on
the
diagnosis
Diagnosis Diagnosis
before
MRI
after
MRI
Cases
with
normal
MUE
(14)
MUE
(14)
MRI
(19)
Probable
MS
(4)
Probable
MS
(4)
Myelitis
(1)
Myelitis
(1)
Cases
with
MRI
Definite
MS
(6)
Definite
MS
(6)
suggestive
of
Probable
MS
(4)
Definite
MS
(4)
MS
(14)
MUE
(4)
Probable
MS
(4)
Table
7
Diagnosis
in
MUE
patients
after
follow-up
MUE
21
(37%)
Definite
MS
15
(26%)
Probable
MS
8
(14%)
Other*
6
(11%)
Acute
myelopathies
7
(12%)
Total
57
(100%)
*Includes
4
cases
of
amyotrophic
lateral
sclerosis,
1
case
of
spondylosis
and
1
case
of
neurobrucellosis.
A
spinal
cord
lesion
was
identified
together
with
the
cerebral
lesion
in
9
cases.
3.
Normal
cerebral
and
spinal
MRI
was
found
in
19
cases,
14
of
whom
were
MUE
after
a
mean
follow-up
of
26
months
(no
case
was
suggestive
of
MS).
Four
other
cases
were
considered
clin-
ically
as
possible MS
but
MRI
was
normal
and
clinical
follow-up
(6,
14,
24
and
84
months)
remained
unchanged.
The
remaining
case
corre-
sponded
to
a
patient
with
acute
myelopathy.
Diagnosis
(Table
7).
After
the
follow-up
and
complementary
examinations
including
MRI,
21
patients
remained
MUE,
15
patients
had
definite
MS,
8
probable
MS,
4
cases
were
amyotrophic
lateral
sclerosis
(included
as
MUE
because
initial
clinical
or
EMG
findings
were
not
conclusive),
1
case
was
myelopathy
caused
by
cervical
spondy-
losis
(included
as
MUE
because
computed
tomo-
graphic
study
and
a
myelography
were
reported
as
normal
on
the
initial
evaluation),
and
1
case
was
myelopathy
caused
by
brucella
(included
as
MUE
because
of
a
negative
initial
serologic
study).
The
7
remaining
cases
were
acute
myelo-
pathy.
Taking
into
account
only
the
chronic
cases,
21
of
50
(42%)
patients
were
MUE,
23
of
50
(46%)
were
definite
or
probable
MS
and
6
of
50
had
other
diagnosis
(12%).
Clinical
course.
The
clinical
course
in
7
pa-
tients
was
acute
(less
than
1
week)
and
evolution
was
monophasic,
being
known
as
"myelitis".
Thirty-five
patients
had
an
insidious
onset
of
symptoms;
in
26
the
course
was
chronic
and
progressive,
in
5
chronic
and
stable
and
in
4
it
was
chronic
but
regressive.
The
remaining
15
cases
had
a
chronic
course
with
bouts.
According
to
the
criteria
of
Paine
et
al
(5)
recovery
was
good
in
13
patients,
regular
in
31
MYELOPATHY
AND
MRI
459
and
poor
in
13.
Four
patients
died
(2
because
of
amyotrophic
lateral
sclerosis,
1
from
MS
and
asthma
and
1
from
MUE
caused
by
cardiorespi-
ratory
arrest).
Discussion
Although
myelopathies
of
unknown
etiology
are
relatively
frequent,
very
little is
known
about
their
etiology.
The
problem
is
quite
different
if
we
con-
sider
acute
and
chronic
myelopathy
separately.
Acute
myelopathy
not
caused
by
compressive
lesions
is
a
syndrome
and
may
be
caused
by
many
entities
(6,
7).
They
therefore
have
a
heter-
ogeneous
prognosis.
In
most
such
cases
the
dis-
ease
is
idiopathic
and
probably
autoimmune
(8).
The
incidence
of
MS
in
this
group
is
low
(9,
10).
In
our
series,
none
of
the
7
cases
have
developed
MS
and
in
the
4
cases
in
which
MRI
was
per-
formed,
this
did
not
suggest
MS
in
any
patient.
Chronic
myelopathy
made
up
27%
of
all
cases
seen
over
a
10-year
period
(72
of
264).
No
signs
or
symptoms
helped
in
the
diagnosis
except
that
patients
with
bouts
more
often
developed
MS.
The
prognosis
was
regular
or
poor
in
a
great
percentage
of
patients.
In
previously
described
series,
chronic
myelo-
pathy
has
been
observed
to
evolve
over
many
years,
thus
explaining
the
reason
for
only
one
necropsic
series
in
the
literature
to
date.
In
1955
Marshall
(3)
examined
35
necropsies
of
MUE
cases
and
was
able
to
diagnose
100%.
Twelve
of
the
35
(34%)
presented
MS
and
11
had
tumors.
In
another
clinical
series
of
52
patients
with
MUE,
27
(54%)
were
diagnosed
over
a
10-year
period.
Of
these,
10
were
MS,
7
tumors
and
10
miscellaneous.
If
we
exclude
tumors
(the
high
incidence
of
which
is
probably
explained
by
the
diagnostic
techniques
available
in
this
period)
the
global
incidence
of
MS
is
12
of
24
in
the
necrop-
sic
series
and
10
of
45
in
the
clinical
series,
thus
totalling
22
of
69
cases
(32%).
In
1971,
Garde
et
al
(11)
examined
45
cases
of
MUE.
Diagnosis
was
obtained
in
44.5%,
of
whom
16%
were
definite
MS
and
22%
probable
MS
cases.
Diagnosis
was
other
in
6.5%
and
55.5%
continued
to
be
MUE.
In
1973,
Hiibbe
et
al
(2)
diagnosed
32
MUE
from
a
total
of
255
spastic
paraparesis,
6
of
whom
were
definite
MS,
one
probable
MS
and
3
had
a
miscellaneous
diagnosis,
thus
making
a
diagnosis
in
10
of
32
patients
(31.2%),
with
MS
being
the
most
frequent.
In
our
series
of
57
MUE,
50
were
chronic
and
7
acute.
After
a
follow-up
of
2.33
years,
21
(42%)
of
the
chronic
cases
continued
to
be
MUE,
23
(46%)
were
definite
or
probable
MS
and
6
(12%)
had
other
diagnoses.
Fifteen
of
the
MS
cases
were
definite
and
8
probable.
Compar-
ing
our
series
and
the
previous
series,
we
can
assume
that
MS
is
the
most
frequent
cause
of
MUE,
and
its
incidence
ranges
between
25-50%
of
the
cases.
The
impact
of
MRI
on
neurologic
diagnosis
has
been
particularly
important
in
the
field
of
spinal
cord
diseases
such
as
in
diagnosis
of
com-
pressive
lesions
or
demyelinizing
diseases
(12,
13).
The
use
of
other
paraclinical
tests
in
the
case
of
MUE
is
limited
and
of
little
predictive
value
(14,
15).
MRI
is
abnormal
in
most
cases
of
definite
MS
(16),
but
its
utility
decreases
in
pa-
tients
of
over
50
years
old,
as
20-30%
of
healthy
individuals
have
anomalies
(unidentified
bright
objects
or
UBO).
Such
UBO
are
observed
in
70-100%
of
patients
with
definite
MS,
although
they
are
not
exclusive
to
this
disease.
According
to
the
new
diagnostic
category
for
MS
proposed
by
Paty
et
al
(16)
(the
MRI-supported
definite
MS
in
individuals
younger
than
40
years),
of
52
MUE
these
authors
found
abnormalities
in
MRI
suggestive
of
MS
in
60%
of
patients.
In
another
series
Miska
et
al
(17)
found
13
of
20
cases
(65%)
and
Miller
et
al
(18)
found
47
of
62
(76%)
in
patients
younger
than
50
years.
In
our
series
we
found
14
of
33
(42%)
MRI
in
MUE
of
the
chronic
type
suggesting
MS.
The
group
of
patients
who
continue
without
a
diagnosis
after
clinical
follow-up
and
explora-
tions
such
as
MRI
is
important
and
must
be
viewed
as
a
syndrome
with
many
etiologies:
viruses
(19),
toxins
(20),
hereditary
disorders
(21),
vascular
problems
(22),
lateral
primary
scle-
rosis
(21,
23),
MS
undiagnosed,
nutritional
defi-
cits
(24),
inflammatory
lesions
(25),
and
others.
Our
study
suggests
that
clinical
findings
do
not
help
to
establish
diagnosis,
while
the
clinical
fol-
low-up
and
MRI
help
to
diagnose
50%
of
pa-
tients,
the
majority
with
MS.
Clearly,
necropsic
460
MARTI-FABREGAS
ET
AL
studies
are
needed
to
more
fully
understand
the
problem
of
MUE.
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Address
Joan
Marti-Fabregas,
M.D.
Hospital
de
la
Santa
Creu
i
Sant
Pau
Servei
de
Neurologia
Avda.
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Antoni
M.
Claret,
167
08025
Barcelona
Spain