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... 22-year-old married female presented with gradual onset weakness of the right side of the body since the last one year, and also inability to speak and loss of vision for the same duration. She was diagnosed as tubercular meningitis one-and-a-half year back, and now was on anti-tubercular drugs under DOTS category II. Her general physical examination was normal. Neurology examination revealed that she was mentally retarded with an IQ of 35, and global aphasia. There was right-sided hemiparesis, power being 3/5 with exaggerated DTJ, and plantar extensor on the right side. Cranial nerve examination revealed that she was totally blind with absent finger counting for both eyes, and absence of projection of rays and perception of light. Fundus examination revealed bilateral secondary optic atropy with normal foveal response. Complete blood count including ESR was normal. ANA, rheumatoid factor, VDRL, and HIV tests were negative. CSF showed cell count of 250/cumm, predominantly lymphocytes, protein was 47 mg% and sugar was 65 mg%. Visual evoked potential revealed no response in both the eyes and bilateral visual pathway dysfunction. MRI brain showed panencephlomalacia in the left temporo-parietal region (Fig. 1). Caseous granulomatous lesions seen in suprachiasmatic region (Fig. 2) and over the right cerebellar region hemisphere (Fig. 3). Similar lesions were seen in the right and left inferior frontal lobe. Bilateral optic nerves were of normal morphology, intensity, and course (Fig. 4). Lateral ventricles and 3rd ventricle were dilated, 4th ventricle was grossly normal, suggestive of communicating hydrocephalus. There was evidence of pachymeningitis. Tuberculosis is still widely prevalent in India. With modern therapy, the survival rate in tuberculous meningitis is now increasing. As a result, neuro- ophthalmic complications which were less common due to early mortality several years ago, are now reasonably frequent. Although tuberculoma of the central nervous system (CNS) is rare in developed countries, in developing countries such as India, the incidence of tuberculoma is as high as 20% 1 . A high incidence of ophthalmologic abnormalities occur in patients with intracranial tuberculomas, even though the lesions do not directly involve the central visual pathways. The most common abnormalities are extraocular motor nerve palsies, visual field defects, and impaired visual acuity, all of which are usually secondary to increased intracranial pressure 1 . Papilloedema was found in 34% of cases 2 . Presence of papilloedema indicates obstruction to CSF outflow and consequent rise in intracranial pressure. Ocular palsy was found in 20% cases. Other associated focal neurological signs were seen in 22% cases. This was a late complication of the disease and was usually associated with tuberculomas 3 . Blindness in one or either eye was rare. Compression of the visual pathways by tuberculoma, tubercular arachnoiditis, vascular insufficiency, and prolonged rise in intracranial pressure, or arachnoidal adhesions, were the common aetiological factors 4, 5 . In our case, the blindness was due to compression of the optic nerve chiasma by a tuberculoma. We are grateful to the department of Radiology, Dr Ram Manohar Lohia Hospital for their valuable ...
