Cortical blindness — loss of visual perception arising from bilateral occipital cortical injury with intact peripheral visual apparatus and preserved pupillary light reflexes — is a rare but severe neurological complication of central nervous system (CNS) tuberculosis. Tuberculous meningitis (TBM) induces vasculitis of small and medium-sized cerebral arteries, producing ischaemic infarctions that preferentially involve the posterior circulation, including the basal ganglia, thalami, and occipital lobes. We present a middle-aged male weaver with a history of pulmonary tuberculosis at age 13 who presented with 20 days of low-grade fever with evening rise, unilateral headache, diminished vision (reported by attenders; denied by patient — consistent with Anton syndrome), and gait unsteadiness. Examination revealed Grade 2 clubbing, bilateral cerebellar signs, and a striking dissociation between subjective visual denial and objectively impaired visual function. All peripheral visual structures were intact. CSF analysis revealed the classical TBM profile: protein 126 mg/dL, glucose 73 mg/dL (CSF:blood glucose ratio reduced), lymphocyte-predominant pleocytosis, positive CSF globulin, and ADA 12 U/L. CBNAAT was negative. MRI brain demonstrated acute infarcts in bilateral occipital regions, right thalamus, and bilateral cerebellar hemispheres — the hallmark posterior circulation multi-territory pattern of TBM vasculitis. The patient was initiated on four-drug anti-tubercular therapy, adjunctive dexamethasone, and concurrent management of newly diagnosed diabetes mellitus. This case highlights that cortical blindness in TBM may be heralded by Anton syndrome, that CSF analysis demonstrating elevated protein, lymphocytic pleocytosis, and elevated ADA is essential to confirm TBM, and that early initiation of ATT with corticosteroids is critical to limit irreversible vasculitic injury.
Dr. Harshavardhana U. H.1*, Dr. S. Rajkumar2, Prof. Dr. Rathnakumar MD3 (Fri,) studied this question.