The orbit is formed by seven bones and has a volume of 25-30 cc. Orbital contents include the eye ball, blood vessels, lymphoid tissue, fat, and muscles; these structures undergo neoplastic changes in this region. Regardless of their benign or malignant nature, tumors cause neuro-ophthalmic symptoms, such as diplopia secondary to exophthalmos（rarely enophthalmos）, restricted eye movements, decreased visual acuity, and the visual field contraction caused by optic nerve compression. Malignant tumors are classified as primary, invasive, and metastatic types. Notably,lymphomas constitute the most common type of orbital tumors. Post-treatment care is not necessary in patients in whom the lymphoma can be completely removed; however, the occurrence of this event is rare. It often causes optic nerve disorders were tend to occurred by tumors from the paranasal sinuses and nasal cavity. Although overall survival rates of cancer patients may be good,maintaining optimal visual function may not be possible. Furthermore, we consider optic neuropathy caused by radiotherapy and anti-cancer drug treatment.

　Benign tumors or mass lesions within the orbit of an eye are broadly divided into three categories: 1）benign tumors, 2）vascular malformations, and 3）lymphoproliferative diseases,which also include IgG4-related orbital inflammation. These tumors might cause visual disturbances, such as decrease in visual acuity, visual field defect, and diplopia, necessitating important interventions for surgical treatment or steroid therapy. However, a“wait-and-see”approach is generally adopted in cases with little or no ophthalmic symptoms. Extensive care must be taken for differential diagnosis of diseases that could transform to malignancy.

　Post-traumatic neuro-ophthalmologic diseases require appropriate diagnosis and treatment. Cranial base fractures and cranial nerve palsies caused by cerebral hemorrhage are often found in head injuries. Furthermore, the orbital roof and optic canal are prone to bone fractures, causing ocular motility disorders and severe visual impairment, respectively. Orbital trauma is often caused by blunt eye trauma, and traumatic optic neuropathy and orbital fractures typically occur in orbital trauma. Traumatic optic neuropathy causes visual impairment immediately after the injury. If steroids are administered early but are ineffective, optic canal decompression surgery might improve vision. Orbital fractures cause ocular motility disorders and enophthalmos. In particular, trapdoor fractures may be associated with bradycardia due to the oculo-cardiac reflex and require emergency surgery.

　The paranasal sinuses and orbits are adjacent to each other, separated by the orbital plate. Inflammation, cystic lesions, and tumors in the sinuses can spread to the orbit and cause orbital symptoms, including impaired eye movement and visual impairment, which can be serious at times. Visual impairment can occur even in sinus diseases that do not have an obvious tendency to overwhelm or infiltrate the orbit on imaging; therefore, immediate consultation with an otolaryngologist is recommended if there are sinus shadows or a clinical suspicion of a sinus association.

　Orbital diseases often lead to diminished vision and diplopia. Currently, it is important to determine whether the cause of visual acuity deterioration is an optic nerve disorder or not. To this end, the presence or absence of a relative afferent pupillary defect was examined to detect optic neuropathy. Subsequently, central flicker value and visual field examinations were performed. When diplopia is caused by optic neuropathy, it is essential to consider idiopathic orbital inflammation, orbital cellulitis, orbital apex syndrome, IgG4-related eye disease, orbital tumor,thyroid ophthalmopathy, and impairment of both the cranial nerves and the optic nerve.

　Orbital magnetic resonance imaging（MRI）is effective in screening for lesions, and T2 fat suppressed weighted images or short inversion time inversion-recovery imaging should be requested. Contrast-enhanced MRI is effective in evaluating orbital apex syndrome.

　We report a case of papilledema secondary to idiopathic intracranial hypertension with hypertensive retinopathy. A 42-year-old woman with a history of untreated systemic hypertension showed severe bilateral optic disc swelling with retinochoroidal folds involving maculas, as well as retinal hemorrhages, hard exudates, and cotton-wool patches on ophthalmoscopic examination. Magnetic resonance imaging and cerebrospinal fluid evaluation revealed idiopathic intracranial hypertension, and she underwent lumboperitoneal shunt placement. The optic disc findings in this patient mimicked those associated with hypertensive retinopathy-induced disc swelling. We discuss a differential diagnosis of papilledema secondary to idiopathic intracranial hypertension.

　Anti-myelin-oligodendrocyte glycoprotein（MOG）antibody-positive optic neuritis is clinically characterized by ocular pain, papilledema, severe optic nerve edema on magnetic resonance imaging（MRI）, and a good response to corticosteroid therapy. We describe a patient with antiMOG-antibody positive optic neuritis associated with branch retinal artery occlusion, anterior ischemic optic neuropathy, macular serous retinal detachment, and ipsilateral abducens nerve palsy, who showed a poor response to corticosteroid therapy.

　A 69-year-old woman presented with optic neuritis of the right eye. She reported a 2-week history of complete loss of light perception and ocular pain. Ophthalmoscopy revealed an edematous and pale disc with splinter hemorrhages. Ocular coherence tomography revealed macular subretinal fluid. Fluorescein angiography revealed segmental hypofluorescence of the disc and a filling defect of the inferior branch of the retinal artery. Contrast-enhanced MRI revealed severe edema of the entire optic nerve. She received 2 courses of intravenous methylprednisolone therapy（500mg daily for 3 days）and 2 courses of intravenous cyclophosphamide therapy（500mg）. The serum anti-MOG antibody test showed positive results after treatment initiation. She was administered an additional course of intravenous methylprednisolone therapy, which gradually improved her visual acuity to 2/10 one year later.

　Anti-MOG antibody-positive optic neuritis is rarely associated with retinal or optic disc ischemia, serous retinal detachment, and ophthalmoplegia.

　A 74-year-old woman presented to our department with the chief complaints of right visual field narrowing, eye pain, and rapid vision loss. At the first visit, her visual acuity was “hand motion”in the right eye and 1.2 in the left eye. The right eye showed a relative afferent pupillary defect（RAPD）. Restricted ocular motility was observed in all directions. No findings other than bilateral cataract were detected. Head fat-suppressed T2-weighted magnetic resonance imaging（MRI）showed swelling and high intensity from the right retrobulbar optic nerve via the chiasm to the optic tract.

　Based on these findings, optic neuritis was suspected, and a steroid pulse therapy（methylprednisolone 1,000 mg for 3 days）was provided. During the progress, anti-myelin oligodendrocyte glycoprotein antibody（MOG-Ab）was detected in the blood test at the initial visit. It was diagnosed as MOG-Ab-positive optic neuritis and orbital apex syndrome due to the spread of inflammation. After steroid pulse therapy, ocular motility disorder improved rapidly, but visual acuity did not improve; therefore, a second course of the steroid pulse therapy was provided. Head fat-suppressed T2-weighted MRI showed decreased high intensity from the right retrobulbar optic nerve, optic chiasm, and optic tract after the 2nd course of steroid pulse therapy, but visual acuity of the right eye improved only to 0.02.

　MOG-Ab-positive optic neuritis was commonly known to have good visual outcomes; however, it is necessary to consider intractable optic neuritis as in this case.

　A 39-year-old man presented to our hospital with no light perception, pain upon ocular movement, and a positive relative afferent pupillary defect in the left eye at the first visit. A highintensity area was observed near the optic chiasm on contrast-enhanced magnetic resonance imaging, and the patient was diagnosed with optic neuritis. No associated diseases were found in the past medical or family history. Three courses of methylprednisolone steroid pulse therapy and plasma pheresis exchange were provided, but the left visual acuity remained unaltered. All antibodies were negative, but a mutated base pair of mitochondrial gene 11778 was observed. No light perception was present even after 4 years, with maintained visual functions in the fellow eye. This is an atypical case of optic neuritis, and no clinical features correspond to Leber hereditary optic neuropathy. We had to concerns about point mutations in the mitochondrial gene in intractable optic neuropathy.

　We report a case of arteritic anterior ischemic optic neuropathy in a patient who developed contralateral eye involvement during steroid therapy. An 85-year-old woman presented with visual acuity classified as“hand motion”in the right eye and 0.7 in the left eye. Based on a relative afferent pupillary defect and pallid optic disc edema identified on ophthalmological examination,we suspected arteritic anterior ischemic optic neuropathy of the right eye. Intravenous steroid therapy was initiated; however, the patient developed symptoms in the fellow eye. Histopathological evaluation of a temporal artery biopsy specimen revealed inflammatory cell infiltrates and giant cells. Tocilizumab（humanized anti-interleukin-6 receptor antibody）therapy was initiated, and steroid therapy was continued. Approximately on day 100 of the treatment course, her visual acuity stabilized to 0.02 and 0.3 in the right and left eyes, respectively. We conclude that tocilizumab could be a useful adjuvant to steroid therapy to treat severe arteritic anterior ischemic optic neuropathy.

Purpose: To evaluate ocular myasthenia gravis（OMG）treatment response and conversion rate of OMG to generalized myasthenia gravis（GMG）in a neuro-ophthalmology clinic of an ophthalmology unit in a tertiary referral hospital in Indonesia.

Methods: This is a retrospective chart review. Study subjects were new OMG patients who had not received treatment previously. The clinical profile of patients, initial and final treatment regimen, treatment response, final diagnosis, and OMG conversion rate and duration were evaluated. Treatment response was evaluated as improvement in diplopia or ptosis after one month of initial treatment, and were categorized as optimal improvement, partial improvement, unchanged, and inconclusive. OMG conversion rate and duration were determined by evaluating the final diagnosis and were classified as OMG, GMG, and conversion to GMG.

Results: Among the 50 patients with OMG, 74％ were prescribed pyridostigmine monotherapy, while 26％ were prescribed an additional oral steroid as the initial treatment regimen. While the majority of patients（75.9％）experienced improvement, 24.1％ patients showed no change in ocular symptoms following initial treatment administration. Neither the presence of diplopia or limited ocular movement in the initial clinical presentation nor the initial steroid use was associated with treatment response（p≥0.05）. OMG to GMG conversion rate was 12.8％, with a mean conversion duration occurring at 11.9±9.3 months since diagnosis.

Conclusions: The majority of OMG patients experienced improvement following initial treatment regimen administration. While OMG conversion rate was low, conversion to GMG mainly occurred during the first year since diagnosis.