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Chronic unilateral optic neuropathy A magnetic resonance study.

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Chronic Udateral Optic Neuropathy:
A Magnetic Resonance Study
D. Eidelberg, MD,"§ M. R. Newton, FRACP," G. Johnson, PhD," D. G. MacManus, DCR,"
W. I. McDonald, FRCP," D. H. Miller, FRACP," A. M. Halliday, MRCP," I. F. Moseley, FRCR,?
G. S. Heng, FRCS,$ and J. Wright, MD, FRCSS
We studied the clinical, electrophysiological, and magnetic resonance imaging (MRI) features of 20 patients with
chronic unilateral optic neuropathy (CUON):progressive unilateral visual failure lasting a minimum of 6 months. The
patients, 10 male and 10 female, ranged in age from 12 to 77 years (mean 44) and had a mean duration of symptoms of
22 months. All had signs of optic nerve dysfunction. Each patient was studied with MRI using a short TI inversion
recovery (STIR) sequence to delineate the optic nerve from surrounding orbital tissue. Three distinct groups of
patients with CUON were identified using MRI. In the first group (8/20) the optic nerve was compressed by an
extrinsic mass, whereas in the second group (5/20)CUON resulted from an intrinsic tumor of the optic nerve or sheath.
In both groups STIR sequences compared favorabIy with computed tomography in identifying mass lesions. MRI was
superior in delineating distortion of the optic nerve by mass or tumor extension beyond the orbit. In the third group
(7/20) no mass was evident on MRI. However, STIR sequences revealed altered signal (long T1) in clinically symptomatic nerves. In 4 of the patients T2-weighted cerebral MRI disclosed periventricular lesions suggestive of disseminated
white matter disease. We conclude that MRI complements clinical and electrophysiological testing in the assessment of
Eidelberg D , Newton MR, Johnson G, MacManus D G , McDonald WI, Miller D H , Halliday AM,
Moseley IF, Heng GS, Wright J. Chronic unilateral optic neuropathy:
a magnetic resonance study. Ann Neurol 1988;24:3-11
Chronic unilateral optic neuropathy (CUON) refers to
progressive monocular visual failure with signs and
symptoms of optic nerve dysfunction. This may be the
result of optic nerve compression due to a mass and
must be distinguished from atypical retrobulbar neuritis {l, 21, tumors of the optic nerve { 3 , 4 ] ,and infiltrative and vascular conditions [5-7). Because of the potential for dramatic recovery following decompression
{ 8 ] , the identification of a surgically removable mass is
essential. Some workers [9) have recently reaffirmed
the conventional position {lo] that neurosurgical exploration should be undertaken in patients with
CUON suspected of harboring mass lesions, even if
neuroradiological investigations are negative.
With the recent development of specialized magnetic resonance imaging (MRI) techniques for the examination of the anterior visual system, it has become
possible to detect and localize lesions of the optic
nerves [l 1). Conventional MRI of the orbital portion
of the optic nerve is limited by the high image intensity
and chemical shift artifact engendered by orbital fat.
Short TI inversion recovery (STIR) sequences { l l , 12)
From the *NMR Research Group and the tLysholm Radiological
Department, National Hospital, Queen Square, and $Moorfields
and the lDepmment
ogy, Memorial Hospital, New York, N.Y.
suppress the signal from fat and allow high contrast
imaging of the prechiasmal optic nerve. This has
proved especially useful in defining foci of abnormal
signal in cases of optic neuritis at times when conventional MRI and computed tomography (CT) of the
optic nerve have been normal {13}. T o explore the
usefulness of MRI with STIR sequences in the differential diagnosis of CUON, we applied the technique
to the study of 20 patients with this syndrome.
Patients and Methods
Twenty patients with C U O N were studied at the National
Hospital and Moorfields Eye Hospital in London. All had at
least 6 months of progressive monocular visual failure and
signs of optic nerve dysfunction with at least two of the
following: afferent pupillary defect, color desaturation, optic
nerve atrophy, or central scotoma. Patients with a retinal
lesion or clinical evidence of a generalized illness likely to
cause an optic nerve lesion, including multiple sclerosis, were
excluded, as were those with signs of chiasmal involvement.
All patients were evaluated clinically by Goldmann perimetry or confrontational testing. In the majority, the visual
fields were also charted on Bjerrurn's screen. Visual evoked
Received Jun 29, 1987, and in revised form Dec 14. Accepted for
publicarion Jan 30, 1988.
Address correspondence to Professor McDonald, Department of
Clinical Neurology, Institute of Neurology, Queen Square, London
W C l N 3BG, England.
Copyright 0 1988 by the American Neurological Association
potentials (VEPs) were recorded in 17 patients by methods
described elsewhere 114-161.
All patients were studied by CT and MRI. MRI was
carried out on a Picker 0.5-Tesla superconducting system
provided by the Multiple Sclerosis Society. Six or eight
5-mm coronal and axial scans through the orbit were performed using specially designed surface coils and a STIR
sequence optimized to suppress the signal from orbital fat
In patients who proved not to have a mass
lesion additional 5-mm multiaxial slices through the entire
brain were taken using a multislice T2-weighted spin echo
sequence (SE2.000160).
Clinical, electrophysiological, and imaging findings are
summarized in Tables 1 and 2. Pathological or radiological diagnoses are provided when available. Based
upon clinical and imaging findings, the patients fell into
three categories: Group A was defined by compressive
optic neuropathy due to extrinsic mass lesions (Patients 1-8); Group B was defined by intrinsic tumors
of the optic nerve and sheath (Patients 9-13); and
Group C was defined by C U O N without identifiable
mass (Patients 14-20).
Grot@ A
Patients 1 to 8 (6 men and 2 women) with identifiable
mass lesions ranged in age from 1 7 to 77 years (mean
5 l),and the average duration of visual complaints was
17 months. In addition to signs of optic nerve dysfunction, 6 of 8 showed clinical evidence of orbital disease
with proptosis and limitation of ocular motility. In Patients 3 and 6 these signs were absent, but a compressing mass was evident on imaging. Vascular congestion
of the retina was found by ophthalmoscopy in 1 patient, but frank disk swelling was absent. One patient
had a normal optic disk.
The pattern of field loss was variable in this group.
Large irregular central scotomas with extension into
the periphery were found in 3 patients. The remaining
5 patients were found to have field constriction or
depression 171 without isolated scotoma. VEPs were
absent in 3 of the 5 patients studied, while in the
others the waveform was abnormal and degraded.
MRI results are summarized in Table 2. STIR sequences compared favorably with CT in the identification of mass lesions in the orbit and middle fossa. MRI
was particularly useful in demonstrating the distortion
of the optic nerve by extrinsic masses in the orbit, and
in delineating extraorbital extension of tumor. In 5
patients high signal suggestive of obstruction of drainage by mass was noted in the superior ophthalmic vein.
Patient 3, with orbital dermoid, had a poorly defined
lesion on CT (Fig 1A) that was better demonstrated on
MRI (Fig 1B).
4 Annals of Neurology Vol 24 No 1 July 1988
Group B
The ages of Patients 7 to 13 (5 females), with intrinsic
tumors of the optic nerve, ranged from 12 to 54 years
(mean 28) with a mean duration of symptoms of 4.5
Two patients (9 and 10) with optic nerve sheath
meningioma were studied. One had the typical finclings of chronic papilledema and optociliary shunt vessels; in the other, the diagnosis was proved on biopsy.
Both had large asymmetrical central scotomas in the
affected eye with either absent or minimal VEP. STIR
images of Patient 9 disclosed a mass enveloping the
nerve, with foci of low signal corresponding to
calcification. In Patient 10, CT scan demonstrated a
thickened optic nerve (Fig 2A). Abnormally high signal within the enlarged nerve was found with MRI
(Figs 2B, 2C). Three patients with optic nerve glioma
were examined, 2 of whom had clinical evidence of
neurofibromatosis (Patients I 1 and 12). Patient 13 had
progressive proptosis, disk atrophy, and visual failure;
despite an acuity of 6/18, the visual field was only
slightly depressed on the affected eye. In addition to
showing gross optic nerve enlargement and intense sig,nal (Fig 3A), MRI disclosed chiasmal involvement (Fig
3B) that was not suspected clinically or electrophysiologically and that was not evident on CT. Although
both patients with neurofibromatosis complained of
monocular visual failure, subtle abnormalities were
noted in the clinically unaffected eye. MRI of these
subjectively normal eyes showed occult lesions with
high signal intensity suggesting bilateral optic nerve
glioma. VEP was normal in one such case. Chiasmal
thickening without hemianopic field defect was also
noted in Patient 12.
Gro@ C
Patients 14 to 20 (4 men and 3 women), with CUON
without a demonstrable mass lesion, ranged in age
from 34 to 67 years (mean 47) with an average duration of symptoms of 4.2 years. None had orbital signs.
VEPs were abnormal in all clinically affected eyes, with
delayed latencies in 5 and abolished responses in 2.
Two subgroups were identified.
In Patients 14 to 17 (mean age 40 years) VEPs from
both eyes were severely abnormal, although signs and
symptoms were monocular. STIR sequences revealed
focal increase in signal without alterations in nerve
caliber in each symptomatic eye (Fig 4A). Occult lesions in the contralateral optic nerve were evident in L!
of these patients. Cerebral MRI with spin echo sequences revealed multiple periventricular abnormalities consistent with multifocal white matter disease (Fig
4B). CT was normal in all these patients. Analysis of
cerebrospinal fluid revealed a mild pleocytosis in one
(Patient 17) and the presence of oligoclonal bands in
another (Patient 15).
Table 1. Clinical Features of 20 Patients with C UON
Age (yr)/Sex Durationa
Visual Fieldsb
12 mo
15 mo
12 mo
7 5/M
9 mo
5 3lM
36 mo
24 mo
615 Atrophy
6/60 Atrophy
Patchy scotoma
Central scotoma
24 mo
6 mo
6/18 Normal
619 Atrophy
Field depression
Temporal constriction
Peripheral constriction
Constricted to
red only
Temporal pallor Large, irregular
central scotoma
LimitedHorner's syndrome
numb cheek
Central scotoma
Constriction of
inferior temporal field
Field depression
Central scotoma
30 mo
12 mo
2 l/E
10 yr
7 Yr
24 mo
shunt vessels
Slight superotemporal constriction
Mild temporal
616 Atrophy
619 Mild disk swelling; anterior
6/60 Disk swelling;
615 Atrophy
Central scotoma
Central scotoma
Field depression
7 7/F
Scotoma with
preserved inferonasal
Scotoma with
temporal extension
Field depression
5 1/M
2 Yr
20 mo
8 Yr
4 1/M
1 Yr
14 mo
6 mo
15 yr
"Duration of symptoms from time of first complaint.
bMonocularfield of affected eye. All contralateral monocular fields were full.
CUON = chronic unilateral optic neuropathy; RE = right eye; LE = left eye; RAPD = relative afferent pupillary defect; CF
detection; + = present; - = absent; NPL = no perception of light.
= count fingers
Eidelberg et al: Chronic Optic Neuropathy
Table 2. VEP. M R I , and Diagnosis in 20 Patients with CUON
Patient Group
and No.
R sphenoid ridge mass with edema in R
Meningioma of sphenoid
Orbital pseudotumor'
Group A
No response RE
Delayed scotomatous response RE
No response RE
Severe degradation and delay of full field response
No response LE
Not performed
Not performed
Not performed
Intraconal mass in superior R orbit; optic
nerve compression
High signal lesions in medial wall of R orbit and in orbital apex; optic nerve compression
R orbital mass
Small delayed response nasal hemifield LE;no response temporal hemifield
N o response LE
Small asymmetrical response
Bilateral degradation of responses
RE delayed and degraded
Group C
Bilateral delay RE > LE
N o response RE; delay LE
Bilateral delay
Bilateral delay
Delay LE
No response LE; minor reduction in response RE
RE delayed and degraded
L orbital mass with tortuous vessels of varying signal
Mass in L middle fossa with extension into
Mass in L superior orbit with extension into
orbital apex; optic nerve compression
Mass in L inferior orbit; optic nerve compression
Orbital arteriovenous malformationb
Metastatic squamous cell carcinoma'
High signal in L optic nerve
Optic nerve sheath menin
Concentric mass surrounding L optic nerve;
foci of low signal corresponding to
Marked enlargement of R optic nerve with
increased signal; small L optic nerve lesion
Enlarged R optic nerve; small L optic nerve
lesion; chiasmal thickening
Marked enlargement of R optic nerve with
high signal extending into anterior chiasm
Optic nerve sheath meningioma'
R optic nerve lesion; periventricular lesions
Bilateral optic nerve lesions; periventricular
R optic nerve lesion; periventricular lesions
Bilateral optic nerve lesions; periventricular
L optic nerve lesion
L optic nerve lesion
R optic nerve lesion
Group B
Optic nerve gliomasb;
Optic nerve and chiasma
gliomasb; neurofibromatosis"
Optic nerve glioma'
"VEP results refer to clinically affected eyes. Contralateral monocular responses were normal unless otherwise specified
'Radiological diagnosis based on computed tomography or angiography.
'Biopsy-confirmed diagnosis.
"Clinical diagnosis.
'Clinically probable diagnosis (see text).
CUON = chronic unilateral optic neuropathy; VEP
right eye; LE = left eye; MS = multiple sclerosis.
6 Annals of Neurology
Vol 24
visual evoked potential; MRI
No 1 July 1988
magnetic resonance imaging; R
right; L = left; RE
Fig 1. Patient 3. (A)Contrast-enhanced axial computed tomography scan shwing a poorly defined abnormality near the right
orbital apex (arrow). (B) The same lesion on axial magnetic
resonance imaging (IRl,rmuollso).The high signal intensity is
consistent with a fEuidfFlled cavity. The pathological diagnosis
was demoid.
Fig 2. Patient 10. (A)Axial computed tomography scan with
enhancement showing thickening of the ldt optic nerve. (B and
C) Axial and coronal magnetic resonance imaging scans
( l R l , s ~ ~ ~ o showing
l l s o ) tubular enlargement of the nerve with
high signal intensity (arrow).
Eidelberg et al: Chronic Optic Neuropathy
F i g 3. Patient 13. (A)Axial magnetic resonance imaging slice
(IRl,rno/4nlljnishowing an intrinsic optic nerve mass pushing the
right globe forward. The intracanalicularportion of the nerve is
enhrged. (B) The posterior aspect of the mass is contiguous with
the optic chiasm (arrow).
Fig 4. Patient 1 5 . (A) Coronal magnetic resonance imaging
(MRI) slice (IR1,5nn/4n/1jn)showing a focus of high signal in thr
midportion of the right optic nerve (arrow).Multislice sequences
showed a similar lesion on the l&t (not shwn). (B) T2-weighted
cerebral MRI scan (SE2,ooopjn)shmuing periventricular lesions.
Patients 18 to 20 (mean age 56 years) had delayed
or absent VEPs in the affected eye with corresponding
abnormalities on STIR images of the optic nerve. Contralateral eyes were generally unaffected. Patients 18
and 19 had bilateral disk swelling and anterior uveitis
suggestive of sarcoidosis, proven by biopsy in 1 case.
Patient 20 had a 15-year history of visual failure with a
thinned optic nerve noted on CT (Fig 5A). Abnormal
signal within the nerve was noted on STIR images (Fig
5B). In contrast to the other subgroup, none of these
strictly monocular cases had periventricular abnormalities on T2-weighted images of the brain.
The syndrome of CUON is often misattributed to retrobulbar neuritis [I, 9, 10, 171, although the two may
generally be distinguished o n the basis of the history.
Specifically, patients with CUON have a long history
of insidiously progressive visual failure, a situation encountered rarely in optic neuritis { 5 , 17, 181. Nonetheless, sufficient overlap exists between these entities
to make a differentiation by history alone unreliable
{ 1, 191. The identification of patients with mass lesions
is particularly challenging in individuals without disk
swelling or signs of orbital disease (i.e., proptosis, vas-
Annals of Neurology
Vol 24
No 1 July 1988
Fig 5 . Patient 20. (A) Computed tomography scan with contrast. Two contiguous axialscans show thinning of the right
optic nerve. (B) Coronal magnetic reJonance imaging scan
(lRl,jool.iolljo) through the posterior optic nerve showing a unilateral increase in signal (arrow).
cular congestion, and limitation of ocular motility). In
this situation the optic disk may be normal 19, 173, and
perimetry is not entirely specific 19, 203. Thus, even
careful quantitative perimetry is inadequate to identify
compression of the optic nerve in CUON patients.
Compressive optic neuropathy has been studied with
VEP 116, 21, 221 and our findings support the previous conclusion that no specific pattern of VEP abnormality can be totally reliable in distinguishing optic
nerve compression from optic neuritis.
We found MRI with STIR sequences to be the most
useful investigation in the differential diagnosis of patients with CUON. In patients with compression of
the optic nerve due to extrinsic tumor, MRI compared
favorably with CT in detecting the presence of a mass.
MRI was generally superior in delineating the border
of the mass, particularly when there was extension into
the middle fossa. STIR sequences, with suppression of
the signal from orbital fat, provide adequate contrast
between normal and pathological tissue for demonstration of distortion of the optic nerve by mass lesions.
Moreover, STIR sequences have the further advantage
over CT of demonstrating pathological changes in signal within the optic nerve. Thus, this technique may
be useful in detecting causes of CUON intrinsic to the
optic nerve, especially when no mass is evident.
Experimentally, the cardinal pathological finding in
longstanding extrinsic optic nerve compression is focal
loss of the myelin sheath around intact optic nerve
axons 1231. Myelin itself does not contribute to the
proton MR signal because of the relative immobility of
its protons 1243. This may explain why the signal from
compressed optic nerves tended to be normal in spite
of distortion by extrinsic masses.
Intrinsic tumors of the optic nerve pose a more
difficult problem in imaging. Enlargement of the optic
nerve and foramen is a variable finding and may be
quite subtle, even with high-resolution CT 1253. MRI
with STIR sequences provides information regarding
the caliber of the nerve as well as demonstrating pathological changes within the substance of the nerve. In
nerve sheath meningiomas and optic nerve gliomas,
high signal may be evident within the substance of the
nerve, corresponding to a long T1 1113. Vacuolization,
edema, gliosis 126, 271, and malignant infiltration 1281
may all give rise to this change in neural tissues. In
intrinsic tumors of the optic nerve any of these factors
may play a part in the condition either singly or in
combination C291. Irrespective of substrate, this pathological alteration in signal allows for detection and assessment of the extent of such tumors at a time when
clinical findings and electrophysiology are normal or
equivocal. In agreement with previous experience 14,
21, 25, 301, we found that optic nerve gliomas may
infiltrate the chiasm without major change in visual
Eidelberg et al: Chronic Optic Neuropathy 9
fields or evoked potentials. Additionally these tumors
may be multiple, although minor growths may be clinically silent 131. MRI may be used to identify chiasmal
invasion or multiple lesions at an early stage. An
equally challenging diagnostic problem is posed by patients with C U O N in whom there is no discernible
mass. This clinically heterogeneous group may be divided into two subpopulations. Although presenting
with CUON, younger patients may have vague past
histories of other neurological complaints. The subjectively normal eye may be abnormal electrophysiologically with delayed VEP latency and may show altered
signal on STIR sequences. The additional presence of
disseminated white matter lesions on SE sequences
13 l} strongly suggests the possibility of underlying
multiple sclerosis as the cause of chronic visual failure
12, 191. Similar MRI findings have been demonstrated
in 60% of patients with acute optic neuritis 1321. Indeed, based upon these findings we suggest that all
patients with C U O N in whom no mass is identified on
STIR sequences be further investigated with T2weighted spin echo sequences of the cerebrum. If
white matter lesions are present, a diagnosis of probable, but not definite, multiple sclerosis may be made
133, 341. In the absence of mass, older patients with
CUON seem less likely to have signs or symptoms of
disseminated disease, a situation analogous to acute
optic neuritis {35]. Cerebral MRI with T2-weighted
sequences is normal; STIR sequences show abnormalities of only the clinically affected optic nerve. In 2
patients a diagnosis of sarcoidosis was based upon the
presence of disk swelling and uveitis, and this was
proved by optic nerve biopsy in 1 patient. In the final
patient the cause of C U O N was uncertain; chronic
optic neuritis remains a diagnosis of exclusion 111.
In summary, C U O N is still a difficult diagnostic
problem. Application of MRI with appropriate scanning sequences has reduced the need for invasive imaging procedures and blind surgical exploration in individuals with suspected mass lesions. MRI compares
favorably with CT in the identification of orbital
tumors and has the advantage of discerning intrinsic
optic nerve abnormalities in individuals without evidence of compression. MRI may also be useful for the
staging and follow-up of individuals with intrinsic optic nerve tumors. Of those patients without a mass,
some will have evidence of generalized white matter
changes, probably multiple sclerosis. Further refinement of the technique will be needed before MRI
clarifies the mechanism of visual loss in the remaining
The study was supported by a Medical Research Council grant.
David Eidelberg is a Fellow of the Moseley Foundation, Harvard
Medical School, Boston, MA.
10 Annals of Neurology
Vol 24
No 1 July 1988
The nuclear magnetic resonance facility was provided by the Multiple Sclerosis Society of Great Britain and Northern Ireland.
Mr George Abramson assisted in the preparation of the manuscript.
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