We present a case report of bilateral optic neuritis related to meningoencephalitis in an adult. A 62-year-old woman was admitted with sudden bilateral visual loss, headache, and fever. Neurological examination showed no specific findings except light perception on bilateral visual acuities. Cerebrospinal fluid examination and brain magnetic resonance imaging indicated meningoencephalitis and infectious optic neuropathy. She was treated with intravenous methylprednisolone and acyclovir for the infectious optic neuritis. After treatment, her vision improved, such that she could read text up close. Although the infectious source was not confirmed, the imaging test results and clinical symptoms strongly indicated that infection did occur. In conclusion, it is very important for clinicians to perform the necessary tests and initiate appropriate treatment as soon as possible for patients with visual impairment of unknown cause.
Optic neuritis is defined as inflammation that damages the optic nerve. Common symptoms include eye pain and temporary vision loss. Optic neuritis is often idiopathic and can occur in association with demyelinating diseases, other rare autoimmune diseases, infectious diseases, and inflammatory and immune responses to vaccination.
Bilateral optic neuritis associated with central nervous system (CNS) infection is rare in adults. Only a few cases of optic neuritis post-encephalitis have been reported in the recent years.
A 62-year-old woman was admitted with sudden bilateral visual loss since 3 days. She had also had headache, dizziness and fever for 4 days. She was receiving medication for hypertension and had no history of going abroad.
On physical examination, she had a mild fever of 37.8°C. Neurological examination showed no specific findings involving the motor and sensory systems. Meningeal irritation sign was negative, and all functions of cranial nerves were normal. On ophthalmologic examination, she retained some light perception on bilateral visual acuities. The pupils were equal, round, and reactive to light. A relative afferent pupillary defect was not definite in both eyes. Furthermore, there was no limitation or pain on eye movement. Dilated fundus evaluation revealed the presence of blurred disc margins, which led to a suspicion of papilledema (
Routine blood chemistry showed normal results. Additional laboratory tests including those for fluorescent antinuclear antibody (FANA), p-anti-neutrophil cytoplasmic antibody (ANCA), c-ANCA, anti-cardiolipin antibody, anti-beta-2 glucose 6 phosphate isomerase (GPI) antibody, vitamin B1, B6, B12, folate, anti-aquaporin 4 antibody, and paraneoplastic autoantibody were also showed normal results. Tests involving N-methyl-D-aspartate receptor (NMDAR), voltage gated potassium channels, and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) were not performed because of the lack of encephalitis characteristics accompanying the optic neuritis. In contrast, thyroid function tests showed a decreased level of thyroid stimulating hormone of 0.223 uIU/mL, increased anti-microsome antibody level of more than 1,300 U/mL, and increased anti-thyroglobulin antibody level of 83.8 U/mL. However, triiodothyronine (T3) and free thyroxine (T4) levels were within the normal range.
The results showed delayed P100 latencies in full field visual evoked potential (VEP) bilaterally. These findings were indicative of prechiasmatic conduction defect in bilateral VEP pathways. Cerebrospinal fluid (CSF) examination was performed: CSF opening pressure, 15 cmH2O; white blood cell (WBC) count, 140/mm3 (79% lymphocytes); protein, 175.0 mg/dL; and glucose, 64 mg/dL (serum glucose: 115 mg/dL). There was no viable cell on CSF cytology. No oligoclonal band was detected in the CSF. Brain magnetic resonance imaging (MRI) showed diffuse swelling and heterogeneous enhancement in both optic nerves, which suggested infectious optic neuropathy (
She was treated with intravenous methylprednisolone and acyclovir for infectious optic neuritis and meningoencephalitis. After 9 days of treatment, brain MRI showed improved meningoencephalitis and optic neuritis (
There are various possible causes of spontaneous bilateral optic neuritis. First, optic neuritis is often a symptom of demyelinating diseases such as multiple sclerosis or neuromyelitis optica spectrum disorders (NMOSD).
Since it is clinically difficult to identify the cause of atypical optic neuritis, clinicians should try to perform active screening and appropriate treatment. Intravenous corticosteroids have been effective in most optic neuritis patients.
This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science and ICT (NRF-2018R1C1B5086320).
No potential conflicts of interest relevant to this article was reported.
Fundoscopy shows (A) bilateral disc margin (white arrow) blurring and papilledema, (B) improved papilledema.
Brain fat suppressed magnetic resonance imaging (MRI) shows (A) diffuse swelling and heterogeneous enhancement in both optic nerves (white arrows) without swelling of medial rectus muscle (white arrowheads). (B) Brain MRI fluid attenuation inversion recovery (FLAIR) sequence shows multiple hyperintense lesions on both basal ganglia, thalamus, left internal capsule. (C) Diffuse swelling and heterogeneous enhancement in both optic nerves improved after 9 days of treatment in brain fat suppressed MRI, and (D) decreased size of hyperintense lesions in brain MRI FLAIR sequence.