A 31-year-old female, presented with headache, diminution of vision in the right eye, and painful extraocular movement for 3-months. She initially consulted a neurologist for severe headache, followed by vision loss and drooping of the right eyelid, where she was prescribed opioid analgesics and anti-inflammatory drugs. CEMRI was advised, which revealed a hyper-intense lesion in the orbital apex, and the patient was referred to our OPD [Figure-1 a, b]. The drooping of the lid was resolved after the medication and the rest of the complaints were still persisting. The BCVA was 1/60 in the right eye and 6/6 in the left eye. On examination, there was no sign of proptosis, extraocular movements were painful, and without any restrictions. RAPD was present in the right eye and a fundus examination was clinically unremarkable. The systemic examination was clinically unremarkable, with no palpable lymph node. A comprehensive blood analysis (CBC, HIV, HbSAg, HCV, IgG4, C-ANCA, P-ANCA, RA factor, serum ACE, ANA, and HRCT chest was within normal limits (WNL).

The Montoux test was strongly positive with 30 × 25 mm induration after 72 h and.

QuantiFERON TB Gold tested positive. A clinical diagnosis of tuberculous orbital apex.

syndrome was made, and the patient was started on ATT with oral steroids. Patient didn’t take treatment and lost follow-up; one month later, she came with similar complaint and the planned treatment was initiated. She completed a 10-month ATT course (2 months of HRZE + 8 months of HR) with tapering oral corticosteroids as advised by the pulmonologist. At 1- year of follow-up, painful ocular movement was resolved completely, BCVA was similar 1/60 in the right eye with a persistent headache. A Fundus examination revealed right eye temporal disc pallor [Fig. 1-e]. A Repeat CEMRI orbit was advised, and the lesion at right orbital apex was completely resolved [Fig. 1-c].

(a & b) CEMRI T1 axial section showing hyperintense lesion at right orbital apex on initial presentation (c) Resolved lesion at right orbital apex on 1-year follow-up (d) Clinical picture on 1-year follow-up (e) Right disc showing temporal pallor on 1-year follow-up

A 40-year-old male with PL-positive on the left eye, presented with headache, painful extraocular movement, diminution of vision, and drooping of the left eyelid for 1 week. On examination, there was no sign of proptosis, with a mild limitation of extraocular movement in up gaze and down gaze. RAPD was present in the left eye with optic disc edema, systemic examination was clinically unremarkable. CECT orbit and blood investigations were advised but the patient denied it and lost follow-up. One week later, he came with a loss of vision in his left eye (PL-negative), CECT revealed swelling and edema in the left optic nerve and extraocular muscles suggestive of orbital inflammatory disease [Fig. 2-a, b]. He denied blood investigation, so IVMP pulse therapy was started immediately (5 cycles every 21 days). Drooping of the lid, painful and limited movement were improved without vision salvage (PL-negative) after complete pulse therapy. Two years after the completion of pulse therapy he came with a headache and painful ocular movement, showing signs of recurrence.

(a & b) CECT Orbit left eye showing swelling in optic nerve and extraocular muscle (c) Montoux test-24 × 26 mm (strongly positive) (d) Clinical picture on 1.8-year follow-up

The detailed blood investigation revealed CBC, HIV, HbS, HCV, IgG4, C-ANCA, P-ANCA, RA factor, Serum ACE, ANA, QuantiFERON Tb Gold, and HRCT chest within normal limits (WNL). The Montoux test was strongly positive with 24 × 26 mm induration after 72 h [Fig. 2-c]. Thus, based on strong montoux positive, ruling out other orbital inflammatory diseases a clinical diagnosis of orbital tuberculosis was made, and he had completed 6 months of ATT (2 months of HRZE + 4 months of HR) with tapering oral corticosteroids as advised by the pulmonologist. After ATT completion, an 18-month follow-up revealed total resolution of ocular symptoms and no signs of recurrence [Fig. 2-d].