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International Journal
of Ophthalmology
2017; 10(9): 1477-1478
·Letter to the Editor·
Optic perineuritis simultaneously associated with
active pulmonary tuberculosis without intraocular tuberculosis
Won Yeol Ryu, Jong Soo Kim
Department of Ophthalmology, Dong-A University College of Medicine,
Busan 602-715, Korea
Correspondence to: Won Yeol Ryu. Department of Ophthal-mology, Dong-A University College of Medicine, 26, Daesingongwon-ro, Seo-gu, Busan 602-715, Korea. wyryu@dau.ac.kr
Received: 2017-04-24
Accepted: 2017-06-20
Citation: Ryu WY, Kim JS.
Optic perineuritis simultaneously associated with active pulmonary tuberculosis
without intraocular tuberculosis. Int
J Ophthalmol 2017;10(9):1477-1478
Dear Editor,
Otic perineuritis is a rare inflammatory disorder involving the optic nerve
sheath and its adjacent tissues. This condition shows dramatic responses to
steroid treatment, although relapse is common. Additional characteristics of
optic perineuritis include the sparing of central vision on a visual field
test, relatively good initial visual acuity, and optic disc edema[1]. Most cases are idiopathic, although some rare cases
have been associated with specific infections, such as syphilis and viral
infections, and autoimmune disorders including Wegener’s granulomatosis,
sarcoidosis, and giant cell arteritis[1-2]. The presentation of optic perineuritis has also been described during
tuberculosis treatment[3]. However, optic
perineuritis simultaneously associated with active pulmonary tuberculosis has
never been published. Here, we report the case of an otherwise healthy woman
who presented with optic perineuritis associated with active pulmonary
tuberculosis without intraocular tuberculosis.
A 39-year-old woman presented with ocular pain and visual loss in her
right eye lasting for one week. Her medical history was otherwise unremarkable, with no immunological
problems. Her corrected visual acuity was 20/20 in both eyes, with a right
afferent pupillary defect. The anterior segment and vitreous were normal with
no cell infiltration. Color vision was intact in each eye. Ocular motility was within normal limits, but
severe pain was
reported during gazing. Funduscopic examination demonstrated optic disc edema
in the right eye (Figure
1). Automated visual
field testing showed a superotemporal field defect and reserved central field in the right eye
(Figure 2). Magnetic
resonance imaging (MRI) demonstrated an enhanced posterior sclera and weakly
enhanced optic nerve sheath in the right eye (Figure 3).
Figure 1 Right disc edema with a normal left optic disc.
Figure 2 The automated visual field shows a superotemporal defect in the right
eye and a normal visual field in the left eye.
Figure 3 Magnetic resonance imaging scans of the orbit, with contrast infusion
and fat suppression, showing an enhanced posterior sclera (A-C) and weakly
enhanced optic nerve sheath (D).
Figure 4 Chest radiograph showing ill-defined focal patchy consolidation in the
right apex (A), and high-resolution computed tomography of the chest
demonstrates multiple centrilobular nodules in the right apex (B).
Cerebrospinal fluid analysis did not show evidence of infection or
malignancy. Laboratory tests, including those to measure erythrocyte
sedimentation rate, C-reactive protein, anti-nuclear antibody, angiotensin-converting
enzyme, anti-neutrophil cytoplasmic antibody, complement, syphilis and viral
serology, renal and liver function, and other blood parameters, showed normal
results. Chest
radiology revealed an ill-defined focal patchy consolidation in the right apex
(Figure 4A).
High-resolution computed tomography of the chest showed multiple centrilobular
nodules in the right apex (Figure 4B). These findings were suggestive of active pulmonary tuberculosis.
Repeated acid-fast bacillus smear and culture were negative, although real-time
polymerase chain reaction of bronchial wash material showed a positive
diagnostic result for Mycobacterium tuberculosis.
A diagnosis of optic perineuritis associated with active pulmonary
tuberculosis was made. The patient was treated with 1.0 g of intravenous
methylprednisolone every day for 3d, followed by oral prednisolone 1 mg/kg·d
for 11d with subsequent tapering for 6wk. In addition, treatment for pulmonary
tuberculosis was initiated with the combination of isoniazid, rifampin, ethambutol,
and pyrazinamide. Ten days after undergoing treatment for pulmonary
tuberculosis, drug-induced hypersensitivity to isoniazid and rifampin
developed. Eventually, the medications for pulmonary tuberculosis were replaced
by pyrazinamide, kanamycin, and levofloxacin.
The patient’s symptoms of ocular pain and visual loss started to
dramatically improve after she received intravenous methylprednisolone for 3d.
Two months after her initial presentation, the optic disc edema had resolved
and her visual field was recovered. The patient has been observed for 12mo without ocular
complications and visual or
tuberculosis relapse.
Optic perineuritis can be difficult to clinically differentiate from optic neuritis, as
both disorders may present with acute visual loss with eye pain, pain with
ocular movement, and a swollen optic disc[1]. MRI
findings of enhancement around the optic nerve, termed the “tram tract” on
axial cuts and a “doughnut” on coronal cuts, can aid in diagnosing optic
perineuritis and differentiate this condition from optic neuritis[1-2]. In the patient described here, enhancement
around the optic nerve was mild. However, MRI were showed enhanced posterior
sclera, suggesting orbital inflammation. Ohtsuka et al[4] reported that enhancement of the adjacent
posterior sclera was observed in a patient with optic perineuritis. In addition, this
patient clinically presented with acute visual loss, pain with ocular movement, and optic disc edema, as
well as sparing of the central vision and normal color vision. These findings are typical clinical features of optic
perineuritis[1], and this patient dramatically responded to
steroid treatment.
The majority of optic perineuritis cases are idiopathic, and causes related to inflammation or
infection are very rare[1]. Jacob et al[3] reported a case that presented with optic perineuritis during treatment for tuberculosis, and the
authors presumed that the etiology may have been caused by dysimmune neuropathy
rather than infection or toxicity due to anti-tuberculosis treatment. In our
case, optic perineuritis simultaneously presented with active pulmonary tuberculosis in an
otherwise healthy adult; therefore, we believe that this case differs from that
of Jacob et al[3], with each case showing a
different pathogenesis.
The mechanism for the simultaneous presentation of optic perineuritis and pulmonary tuberculosis in this case is
unknown. However, posterior scleritis can occasionally be caused by systemic
infection, and inflammation of the posterior sclera may extend to the optic
nerve sheath. Gupta et al[5] reported a
patient with isolated posterior scleritisand tuberculosis in the cervical lymph
node; their case also seemed to manifest as intraocular tuberculosis, although
our patient did not exhibit intraocular inflammation.
This is the first reported case of optic perineuritis simultaneously
associated with active pulmonary tuberculosis without intraocular tuberculosis.
In particular, this condition developed in an otherwise healthy and
immunocompetent adult. Thus, it is important to be aware of accompanying
infective or inflammatory disorders when diagnosing optic perineuritis.
ACKNOWLEDGEMENTS
Conflicts of Interest: Ryu WY, None;
Kim JS, None.
REFERENCES
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