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Optic Perineuritis
Clinical and Radiographic Features
Valerie Purvin, MD;
Aki Kawasaki, MD;
Daniel M. Jacobson, MD
Arch Ophthalmol. 2001;119:1299-1306.
ABSTRACT
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Background Optic perineuritis is an uncommon variety of orbital inflammatory disease
that is distinct from demyelinating optic neuritis.
Objective To describe the clinical and radiographic features of idiopathic optic
perineuritis, with particular emphasis on those features that help to distinguish
this condition from optic neuritis.
Methods We reviewed the medical records of 14 patients with optic perineuritis
who were seen in 2 neuro-ophthalmology clinics.
Results Patients ranged in age from 24 to 60 years; 5 were older than 50 years.
All patients had visual loss, eye pain, or both. The visual acuity was 20/20
or better in 8 of the 15 eyes. The results of visual field testing were normal
in 2 eyes, and a paracentral scotoma or an arcuate defect was seen in 7. Magnetic
resonance imaging scans demonstrated circumferential enhancement around the
optic nerve, sometimes with intraorbital extension. Response to corticosteroids
was dramatic; however, 4 patients had a relapse with lowering of the dose.
Conclusions In contrast to those with optic neuritis, patients with optic perineuritis
are often older at onset and are more likely to show sparing of central vision.
Magnetic resonance imaging scans demonstrate enhancement around, rather than
within, the optic nerve. Response to corticosteroids is more dramatic than
in patients with optic neuritis, and patients are more likely to experience
recurrence after stopping treatment.
INTRODUCTION
OPTIC perineuritis (OPN), also termed perioptic neuritis, is an uncommon
inflammatory disorder involving the optic nerve sheath. Historically, the
term has been used to describe several different clinical entities.1 In recent years, OPN has generally been understood
to represent a form of idiopathic orbital inflammatory disease, in which the
specific target tissue is the optic nerve sheath.2
While most cases are isolated and idiopathic, OPN occasionally occurs as a
manifestation of a specific infectious or inflammatory disorder, such as Wegener
granulomatosis or giant cell arteritis.3
Radiographically, OPN may simulate optic nerve sheath meningioma,4 but clinically it is more likely to be mistaken for
acute demyelinating optic neuritis (ON). In both OPN and ON, patients typically
experience acute monocular visual loss, pain with eye movement, and either
a normal or a swollen optic disc. The natural history of and response to treatment
for these 2 conditions, however, may differ. It is, therefore, important to
identify any clinical and radiographic features that might help in distinguishing
the 2 expediently. To better characterize the clinical features of OPN, we
reviewed the medical records and radiographic studies of 14 affected patients.
We paid particular attention to features that might be helpful in distinguishing
OPN from ON.
PATIENTS AND METHODS
The diagnosis of OPN was made in patients who had an acute optic neuropathy
and/or disc edema plus either radiographic demonstration of enhancement of
the optic nerve sheath or histopathologic evidence of perineural inflammation.
We excluded patients with clinical or radiographic evidence of a more widespread
orbital process (eg, significant exophthalmos or prominent enlargement or
enhancement of extraocular muscles). The presence of subtle orbital abnormalities
was not considered an exclusionary factor. Patients were also excluded if
they had an established systemic disorder associated with orbital inflammation
or if their or a subsequent clinical course evaluation revealed a specific
systemic illness as the cause of their optic nerve sheath inflammation. Patients
were followed up for a long enough period to ensure that an infectious or
neoplastic leptomeningeal process was not present.
We analyzed symptoms, optic nerve function (visual acuity, color vision,
and visual field), optic disc appearance, and radiographic findings. Response
to treatment and long-term course were also studied.
All patients underwent laboratory testing to exclude specific systemic
inflammatory diseases. In all patients, the complete blood cell count, the
erythrocyte sedimentation rate, and the levels of antinuclear antibodies and
angiotensin-converting enzyme were determined; a syphilis serologic test was
performed; and a chest x-ray film was obtained. All patients underwent magnetic
resonance imaging (MRI) of the head and orbits with fat suppression and contrast
infusion. In addition, 7 patients underwent testing for antineutrophil cytoplasmic
antibodies (including all patients with intracranial extension), 3 were tested
for Lyme disease, and 3 underwent a lumbar puncture. A biopsy of the optic
nerve lesion was performed in 2 patients.
RESULTS
The 14 patients included 10 women and 4 men, ranging in age from 24
to 60 years (mean, 41 years; median, 39 years) (Table 1). Five patients were older than 50 years at onset. Ocular
involvement was monocular when first seen in 13 patients and binocular in
1 (patient 12). Thus, data for 15 eyes were analyzed.
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Table 1. Clinical Features When Initially Seen*
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All patients had symptoms of visual loss, eye pain, or both. Eight patients
had visual loss and eye pain that was commonly exacerbated by eye movement.
Pain was absent in 1 patient (patient 2) at onset but developed 3 months later.
Pain was not associated with subjective visual loss in 5 eyes (patients 1,
4, 9, 12, and 13). Visual loss was variably described as blurring, dimming,
splotches, or a "spot" in vision.
Pertinent findings are summarized in Table 1. The visual acuity when first seen was 20/20 or better in
8 (53%) of the 15 eyes. The results of the visual field examination were normal
in 2 (13%) of the 15 eyes. Three eyes demonstrated an arcuate defect, and
4 had a paracentral scotoma. A central scotoma or central depression was found
in 3 eyes, and only a remaining peripheral island was seen in 2. Disc edema
was observed in 10 eyes. Mild motility disturbance was found in 4 eyes (patients
5, 7, 9, and 14). Mild ptosis was seen in 2 patients (patients 6 and 9), and
developed later in the course of 2 additional eyes (patients 2 and 14).
Magnetic resonance imaging scans demonstrated enhancement around the
intraorbital optic nerve in 13 patients. In 1 patient (patient 14), enhancement
appeared to involve the full thickness of the optic nerve, and in this patient
the diagnosis was based on pathologic examination results. In another patient
(patient 8), the MRI scan showed sheath and optic nerve enhancement. There
was intracranial extension in 3 patients (patients 2, 8, and 14). None of
the scans revealed white matter lesions.
All patients had normal laboratory test results, except 1 (patient 7)
in whom the fluorescent treponemal antibody absorption test result was weakly
positive. In this patient, the results of confirmatory serologic tests (the
VDRL test and microhemagglutination–treponemal pallidum) and the cerebrospinal
fluid fluorescent treponemal antibody absorption test were negative. A biopsy
specimen of the optic nerve lesion in 2 patients (patients 2 and 14) showed
acute and chronic inflammatory changes without granulomas or vasculitis (Figure 1). All 3 patients with intracranial
extension underwent an expanded evaluation for granulomatous disease, including
testing for antineutrophil cytoplasmic antibodies (perinuclear–antineutrophil
cytoplasmic antibody and cytoplasmic–antineutrophil cytoplasmic antibody)
and chest radiography. The results of these studies were normal.
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Figure 1. Patient 14. An excisional biopsy
specimen of the left optic nerve of a 42-year-old otherwise healthy woman
who experienced progressive painful visual loss in the affected eye over 6
months, unresponsive to corticosteroids. A malignant optic nerve glioma was
suspected. A, A low-magnification axial photomicrograph of the optic nerve
and sheath complex showing marked thickening of the perioptic meninges (M)
and, to a less dramatic extent, the pia mater (white arrow) due to fibrosis
and inflammatory infiltration. The infiltrate also extends into the pial septa
(black arrow) (hematoxylin-eosin, original magnification x10). B, There
is marked expansion of the pial septa (S) by the chronic inflammatory cell
infiltrate. The parenchyma of the adjacent optic nerve is slightly infiltrated
by lymphocytes (hematoxylin-eosin, original magnification x10).
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Twelve patients were treated initially with prednisone, typically 60
or 80 mg/d, and 2 were treated initially with indomethacin. All experienced
dramatic relief of eye pain, usually within 24 hours of starting treatment,
and prompt improvement of vision (within days of initiating corticosteroid
therapy). Four patients had a relapse when the corticosteroid dose was reduced,
necessitating the use of additional treatment modalities, including intravenous
methylprednisolone (2 patients), peribulbar corticosteroids (1 patient), azathioprine
(2 patients), and radiation therapy (2 patients). The final visual acuity
was 20/25 or better in 12 (80%) of the 15 eyes. Two patients (patients 2 and
14) experienced a poor visual outcome, in each instance associated with a
delay in initiating corticosteroid treatment (Table 2).
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Table 2. Clinical Course*
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Follow-up intervals ranged from 1 month to 6 years (mean, 12
months; median, 9 months) (Table
2).
PATIENT 1
A 26-year-old woman developed right retro-orbital pain exacerbated by
eye movement and mild photophobia 2 weeks following an upper respiratory tract
infection. The results of an ophthalmologic examination 2 weeks after onset
revealed right optic disc edema and subjective color desaturation; otherwise,
the test results of optic nerve function were normal. An MRI scan showed enhancement
around the right optic nerve (Figure 2).
Two weeks later, she began treatment with prednisone, 40 mg/d, which was tapered
over 12 days. This brought prompt relief of pain, but the visual acuity declined
from 20/20 to 20/40 OD. Eight weeks after the onset of symptoms, she was seen
in neuro-ophthalmologic consultation. Her visual acuity was 20/80 OD and 20/20
OS. Goldmann perimetry in the right eye showed an absolute inferior arcuate
scotoma plus a smaller superior scotoma (Figure 3). The visual field in the left eye was normal. There was
a +2 right relative afferent pupillary defect. The results of external biomicroscopy
and ocular motility examinations were normal. The results of a fundus examination
revealed moderate hyperemic right optic disc edema and a normal left optic
disc (Figure 4).
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Figure 2. Patient 1. Magnetic resonance
imaging scan of the head and orbits, with contrast infusion and fat suppression.
A, The axial view shows enhancement around the right intraorbital optic nerve
with some "streakiness" of the surrounding orbital fat. R indicates right
side. B, The coronal view confirms that the enhancement is around, rather
than within, the optic nerve.
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Figure 3. Patient 1. Goldmann perimetry
in the right eye shows an absolute inferior arcuate scotoma and a smaller
less dense scotoma in the superior Bjerrum area. The field in the left eye
is normal.
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Figure 4. Patient 1. Fundus photographs
taken 8 weeks after the onset of symptoms show persistent right optic disc
edema (A) and a normal left optic disc (B).
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Additional laboratory testing included the determination of the complete
blood cell count, the erythrocyte sedimentation rate, and the levels of antinuclear
antibodies and angiotensin-converting enzyme and the performance of a syphilis
serologic test and chest radiography; the results of all tests were normal
or negative. Corticosteroid treatment was reinstituted, starting this time
at 80 mg/d and decreasing by 20 mg/wk. The results of reexamination 4 weeks
later showed improvement of the visual acuity to 20/20 OD. The visual field
was also much improved, showing only mild central depression. Right optic
disc edema had resolved, and the disc was mildly pale.
PATIENT 2
A 37-year-old previously healthy man experienced "foggy" vision in his
left eye accompanied by a few sparkles of light. He had a sensation of heaviness
of the involved eye but no actual eye pain and no discomfort with eye movement.
The results of an eye examination 2 weeks after onset showed a visual acuity
of 20/60 OS, with a 0.9–log unit relative afferent pupil defect and
normal optic discs. Goldmann perimetry in the left eye revealed mild central
depression and a small scotoma inferior to fixation.
Laboratory test results were all normal or negative, and an MRI scan
of the head and orbits was interpreted as normal. Reexamination 5 weeks later
showed no change in visual acuity, but visual field testing revealed mild
additional central depression in the left eye. He received a course of prednisone,
80 mg/d, which was tapered over 4 weeks. Optic nerve function improved; however,
2 months later he experienced abrupt onset of severe left retro-orbital pain
with worsening of vision. He did not seek medical attention until 1 month
later, at which time an MRI scan demonstrated enhancement around the apical
portion of the left optic nerve with extension intracranially (Figure 5). In retrospect, enhancement around the apical optic nerve
could be identified on his initial scan as well.
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Figure 5. Patient 2. A magnetic resonance
imaging scan with contrast infusion obtained 4 months after the onset of visual
symptoms. A, The coronal view through the orbital apex shows enhancement around
the left optic nerve. There is also mild enlargement and enhancement of extraocular
muscles. B, The coronal view more posteriorly demonstrates extension of the
inflammatory process intracranially to the anterior cavernous sinus and along
the planum sphenoidale.
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His visual acuity had declined to hand motions OS, with a large dense
central scotoma. He enjoyed only a modest response to intravenous methylprednisolone
followed by oral prednisone. His vision worsened again 2 months later, at
which time he received a course of radiation therapy consisting of 2520 rads
(25.2 Gy) in 14 fractions. Recurrence of pain 4 months later was treated with
low-dose alternate-day prednisone plus azathioprine. He has been stable for
18 months, since beginning this regimen.
COMMENT
Optic perineuritis was first described by Edmunds and Lawford5 in 1883. These researchers distinguished between 2
forms of the disorder: exudative and purulent. The exudative form consisted
of a localized nonsuppurative pachymeningitis.1
The purulent form was associated with leptomeningitis that had extended to
involve the subarachnoid space surrounding the optic nerves. In many such
cases of OPN, optic nerve function has been said to be normal, an observation
consistent with the concept that the inflammatory infiltrate is loosely organized
around the optic nerve.
More recently, the term OPN has been used to designate a form of orbital
inflammatory disease in which the main focus of the inflammatory response
is the optic nerve sheath.6 Other focal forms
of orbital inflammatory disease include periscleritis, orbital myositis, and
dacryoadenitis.7 Dutton and Anderson4 described the clinical, radiographic, and pathologic
features of 4 patients with OPN in whom enlargement of the intraorbital optic
nerve was thought to represent an optic nerve sheath meningioma. Biopsy specimens,
however, demonstrated inflammatory infiltration of the dural sheath in 2 patients
and dense perineural fibrous tissue in the other 2. None were associated with
a specific inflammatory disorder. Of the 4 patients, 3 differed clinically
from patients with optic nerve sheath meningioma in that head and eye pain
was prominent. Only 1 of the 4 patients was treated with corticosteroids,
which stabilized vision for 6 months until complications led to their discontinuance.
A patient with bilateral idiopathic optic nerve sheath inflammation, described
by Margo et al,8 did not experience a beneficial
response to corticosteroids. A full-thickness biopsy specimen of the more
severely involved optic nerve revealed chronic inflammation of the optic nerve
sheath with vasculitic changes and necrobiotic granulomas. Visual loss was
attributed in large part to secondary ischemic infarction of the optic nerve,
presumably due to circumferential compression of the optic nerve periphery
by the mass of the thickened optic nerve sheath.8
Two similar patients, in whom visual loss was due to vascular occlusion, were
described by Winterkorn et al9; however, a
biopsy was not performed.
The pathologic changes of the optic nerve sheath and the optic nerve
that were present in our patients and in those that have been previously described
suggest that the clinically defined entity of OPN likely encompasses a spectrum
of disorders. Regardless of what unknown process incites the initial inflammatory
process in idiopathic cases, the common pathologic reaction consists of marked
thickening of the optic nerve sheath due to nonspecific fibrosis.4 Various stages of predominantly lymphocytic infiltration
are usually present. In the case reported by Margo et al,8
foci of degenerating (necrobiotic) collagen were present in the optic nerve
sheath. Of the 4 patients described by Dutton and Anderson,4
1 showed granulomatous inflammation in the sheath. Visual loss in those patients
in whom a biopsy of the optic nerve was performed or in whom the optic nerve
was excised correlated with the presence of either optic nerve demyelination7, 10 or infarction.8
Perivascular lymphocytic infiltration of small optic nerve vessels (vasculitis)
has been identified in some patients.7, 11
In most cases of suspected OPN, an optic nerve biopsy is not indicated.
The diagnosis is typically based on a combination of clinical and radiographic
findings. Neuroimaging in patients with OPN typically shows a characteristic
pattern of enhancement around the optic nerve ("tramtrack" on axial views
and "doughnut" on coronal views). In addition, MRI scans in some cases show
streaky enhancement of orbital fat (Figure
2). These radiographic changes are not found in patients with typical
demyelinating ON. In occasional cases of OPN, the substance of the optic nerve
also shows enhancement,12 presumably due to
inflammation of intraneural pial septa as well as the nerve sheath. Two of
our patients exhibited this finding, with histopathologic correlation demonstrated
in 1. In some patients, close inspection may reveal subtle enhancement of
extraocular muscles and/or sclera in addition to the characteristic changes
in the optic nerve sheath (Figure 5).
A careful inspection for these changes may be particularly helpful in cases
in which the perineural findings are subtle or indeterminant and particularly
in those scans that demonstrate intraneural enhancement. Computed tomographic
scanning does not usually provide sufficient spatial resolution to distinguish
perineural enhancement from the intraneural enhancement seen in demyelinating
ON. Recent advances in MRI, specifically the use of dedicated orbital views
with fat suppression and gadolinium, have enabled us to make this distinction.
Accordingly, we suspect that the prevalence of this disorder has been underestimated.
In the pre-MRI era, some cases of OPN may have been diagnosed as being "atypical
corticosteroid-responsive ON."
Based on shared clinical features, patients with OPN are likely to be
misdiagnosed initially as having ON. Similar to those with ON, most patients
with OPN are women (71% [10 of 14 patients] in our series) and most experience
acute monocular visual loss accompanied by eye pain. In patients with both
disorders, eye pain is commonly exacerbated by eye movement. Disc edema is
often present in patients with both conditions (found in 10 of the 15 eyes
in our series). Treatment considerations and prognosis, however, differ for
these 2 disorders, particularly regarding the future development of multiple
sclerosis. Based on our data, we found several features to be helpful in distinguishing
OPN from ON (Table 3).
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Table 3. Features That Distinguish Optic Neuritis From Optic Perineuritis
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The age distribution of patients with OPN is broader, and the average
age is older than in patients with ON. Our patients' age ranged from 24 to
60 years (mean, 41 years). The average age of patients with ON is 33
years; only 15% of cases occur in individuals older than 50 years.13 In contrast, 5 (36%) of our 14 patients were older
than 50 years.
The tempo and pattern of visual loss also differed in our patients compared
with those with ON. In contrast to visual loss in patients with ON, which
usually occurs over several days, visual loss in many of our patients with
OPN progressed for several weeks before they were correctly diagnosed and
treatment was initiated. Although occasional patients with ON demonstrate
sparing of central vision, we found this to be a common pattern in patients
with OPN. The visual acuity was 20/20 in 8 (53%) of the 15 eyes. The results
of visual field testing were normal in 3 eyes; a paracentral scotoma was seen
in 4, and an arcuate defect was seen in 3. Thus, 10 of the 15 eyes demonstrated
sparing of central vision. In contrast, in a study of 103 patients with ON,
Perkin and Rose13 found only 4.2% to have central
sparing. In keeping with their tendency to spare central vision, the degree
of dyschromatopsia was less than typically seen in patients with ON.
Mild motility disturbance, due to extraocular muscle inflammation, is
occasionally a helpful feature. Four of the 14 patients had abnormal ocular
motility, based either on eliciting a history of diplopia or on examination
findings. One of these 4 and an additional patient exhibited mild ptosis in
the involved eye, and 2 others developed mild ptosis later in their course.
These are not typical features of ON (unless there is associated brainstem
involvement due to multifocal demyelinating disease), and their presence in
a patient suspected of having ON should suggest the alternative diagnosis
of OPN.
Finally, the response to treatment may help in differentiating OPN from
ON. Of our 14 patients with OPN, 12 were treated with corticosteroids, and
all demonstrated dramatic relief of pain on initiating treatment, typically
within hours and all within a day. Visual loss also showed prompt recovery.
Relapse following discontinuation of treatment, however, was common. These
features, particularly the recurrence of pain and/or visual loss on corticosteroid
tapering, should suggest a diagnosis of OPN rather than ON. Specific inflammatory
and neoplastic entities, such as sarcoidosis, lymphoma, leptomeningeal carcinomatosis,
and some fungal infiltrations, may demonstrate a similar response to treatment.
These disorders, however, soon declare themselves by demonstrating recurrence
and progression with or without continued corticosteroid treatment.
The prognosis for visual outcome in patients with OPN is generally excellent.
This is greatly influenced, however, by the interval between the onset of
visual loss and the initiation of treatment. In 2 patients with a poor visual
outcome, treatment was delayed by a month or more. The other factor that influences
prognosis is the frequency of recurrent attacks. Initiating treatment with
higher doses of corticosteroids (eg, prednisone, 80 mg/d) and more prolonged
treatment at this level appear to lessen the likelihood of recurrent attacks.
The possibility of OPN should be considered in all patients in whom
ON is diagnosed. Magnetic resonance imaging is particularly important in patients
with clinical findings that are atypical for demyelinating ON. Specifically,
these would include age older than 45 years, sparing of central vision, visual
loss progressing for longer than 2 weeks, persistence of disc edema, recurrence
of pain, and visual loss after discontinuing corticosteroid therapy. Patients
in whom pain is particularly severe or is out of proportion to visual loss
might also be considered in this category. Careful scrutiny, in terms of history
and physical examination, for evidence of orbital involvement (diplopia, subtle
ptosis, and chemosis) may also help to identify these patients.
It is important to accurately distinguish between OPN and ON for 2 reasons.
First, the prognosis is different in these disorders. Patients with ON are
at high risk of developing multiple sclerosis and should be counseled accordingly.
Patients with OPN, in contrast, are not at increased risk for demyelinating
disease but are likely to experience a recurrence of visual loss in the future.
Second, treatment considerations differ for the 2 entities. Corticosteroids
have not been shown to influence the visual outcome in patients with ON and,
therefore, many patients with ON are managed expectantly (ie, without treatment).
Patients with OPN, however, will continue to lose vision, in some cases irreversibly,
unless treated with corticosteroids or other anti-inflammatory agents. Furthermore,
the dosage and route of administration differ. The recommended regimen for
OPN (oral prednisone, 80 mg/d) is contraindicated in patients with ON because
of the association of this treatment with recurrences of ON. On the other
hand, the rather short (2-week) course of corticosteroid treatment used in
patients with ON is not long enough to achieve lasting remission in most patients
with OPN.
AUTHOR INFORMATION
Accepted for publication February 1, 2001.
Corresponding author and reprints: Valerie A. Purvin, MD, Midwest
Eye Institute, 201 Pennsylvania Pkwy, Indianapolis, IN 46280 (e-mail:
Vpurvin{at}iupui.edu).
From the Midwest Eye Institute and the Departments of Neurology and
Ophthalmology, Indiana University Medical Center, Indianapolis (Drs Purvin
and Kawasaki); and the Marshfield Clinic, Marshfield, Wis (Dr Jacobson).
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