Korean J Ophthalmol Vol.22, No.3, 2008 Fig. 5. Visual field test. A right homonymous upper quadrant defect was noted after four months of added treatment. unilateral and appear predominantly in the posterior pole as solitary or multiple amelanotic lesions.5 The disease is categorized as follows based on examination findings: Stage1 - fever, malaise, headache without cranial nerve impairment Stage 2 - single cranial nerve impairment due to basilar disease, the presence of paresis and focal seizures Stage 3 - patients are comatose or stuporous and have marked neurologic impairment, including multiple cranial nerve palsies, hemiparesis, or paraplegia this disease stage has a high rate of neurologic sequelae or death despite therapy.2 Moreover, third nerve and optic nerve involvement are also significantly associated with tubercular meningoencephalitis stage 3. Generally, tubercular meningoencephalitis stage 3 is associated with neuro-ophthalmic features, and it is more common in the elderly. This may be because of the better survival ability of older children and therefore a greater chance of wide-ranging involvement. In addition, after sutural fusion at 24 months, increased intracranial pressure is likely to further damage the brain, and in older children aggressive host reactions in the form of basal exudates may further contribute.6 In the present case, due to a stuporous mental status, the patient was diagnosed as having stage 3 disease. Ptosis and external ocular movement limitation due to oculomotor nerve impairment also occurred in this patient. He responded well to treatment, but mild neurologic sequelae remained and he developed another visual field defect. The majority of patients with ocular tuberculosis require systemic therapy, and isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin are usually administered. Neuro-ophthalmic feature improvements and choroidal tuberculoma involution 204 to a flat inactive scar can occur given accurate rapid diagnosis and treatment. However, neurologic sequelae may remain despite proper therapy in cases of stage 3 tuberculous meningitis. Thus, the prognosis of tuberculous meningitis is related to the timing of the initiation of appropriate therapy. Delays in diagnosis and treatment result in poor prognoses and severe neurological sequelae. In summary, when a patient with tuberculous meningitis presents with abrupt onset oculomotor nerve palsy, rapid re-diagnosis should be undertaken and proper treatment initiated, because the prognosis is critically dependent on the timing of adequate treatment. References 1. Desai HG, Anklesaria ED. Ophthalmological aspects of tuberculous meningitis. J Indian Med Assoc 196749:429-32. 2. Johnson RT, Griffin JW, McArthur JC. Current therapy in neurologic disease, 7th ed. Philadelphia: mosby, 2005; 158-60. 3. Milla E, Zografos L, Piguet B. Bilateral optic papillitis following mycoplasma pneumoniae pneumonia. Opthalmologica 1998;212:344-6. 4. Kocen RS, Parsons M. Neurological complications of tuberculosis: some unusual manifestation. Q J Med 1970;39: 17-30. 5. Levecq LJ, De Potter P. Solitary choroidal tuberculoma in an immunocompetent patient. Arch Ophthalmol 2005;123: 864-6. 6. Amitava AK, Alarm S, Hussain R. Neuro-ophthalmic features in pediatric tubercular meningoencephalitis. J Pediatr Ophthalmol Strabismus 2001;38:229-34.