Juxtaposed Homonymous Hemianopsia Due to Neurotuberculosis

Tuberculosis (TB) is the leading cause of death from a single infectious agent (1). In 2018, the US national incidence of TB was 2.8 cases per 100,000 persons and Texas is estimated to be the second highest incidence of TB in the United States (12.5%). Among all the reported US cases, 70.2% occurred among non–US-born people, but Asian origin represented 35.3% of all the reported TB cases (2). Extrapulmonary TB is infrequent accounting only for 15% of the cases (1), and a homonymous hemianopsia is a distinctly unusual presentation for TB. We present a case of extrapulmonary TB presenting with juxtaposed homonymous hemianopic visual field loss. To the best of our knowledge, this is only the second such case in the English language ophthalmic literature. CASE REPORT A 73-year-old Asian man presented with bilateral progressive peripheral vision loss. He had a 4-month history of fine motor dysfunction in his hands, headache, and gait imbalance superimposed on chronic and progressive neurocognitive deficit since 2003. The patient had migrated from East Asia almost 5 decades ago and was highly functioning at previous baseline with a master's degree in plant science. In 2003, the patient was evaluated at an outside hospital in his native Taiwan, and cranial MRI showed mild leptomeningeal enhancement on the left parieto-occipital region (Fig. 1A). Two weeks later, a lumbar puncture (LP) showed normal opening pressure, normal cerebrospinal fluid (CSF) cell count, and “high” CSF protein count. No diagnosis was made, and the patient's neurocognitive status and memory continued to slowly decline. The patient subsequently returned to the United States.FIG. 1.: Comparison of findings in MRI. A. 2003 MRI, T2 showing discrete leptomeningeal enhancement (white arrows). B. 2019 MRI. Upper images are T2 FLAIR showing extensive vasogenic edema in the parietal lobe, much greater on the right side. Lower images are DWI showing the T2 shine-through phenomenon. DWI, diffusion-weighted imaging.Medical history was significant for hypertension, obstructive sleep apnea, primary open-angle glaucoma (POAG), and erectile dysfunction. His medications included vitamin supplements, lisinopril, and topical latanoprost and timolol. He had no reported allergies. He denied smoking, use of alcohol, or recreational drugs. Family history was noncontributory. In 2019, he presented to the neuro-ophthalmology clinic for painless, progressive vision loss in both eyes and worsening neurocognitive function. The best-corrected visual acuity was 20/40 in both eyes. The pupils were isocoric without a relative afferent pupillary defect. Slit-lamp biomicroscopy was normal in both eyes except for nuclear sclerotic cataracts consistent with 20/40 vision in both eyes. Intraocular pressure measured 14 mm Hg in the right eye and 12 mm Hg for in the left eye on topical latanoprost and timolol. The patient had been followed for presumed POAG, and the glaucoma specialist had described a vertical cup-to-disc ratio of 0.8 in both eyes by color and contour ophthalmoscopically. Automated (Humphrey visual field) perimetry showed a right homonymous hemianopia juxtaposed to an inferior arcuate glaucomatous type defect in the right eye and to a possible left-inferior quadrantanopia (Fig. 2). Optical coherence tomography (OCT) of the retinal nerve fiber layer (RNFL) showed superior RNFL loss consistent with superior nerve fiber layer loss. However, the patient's visual field defect (right homonymous hemianopsia) did not correspond to the OCT findings and was not consistent with glaucoma alone.FIG. 2.: Humphrey 24-2 visual fields, RNFL quadrants of the optic nerve OCT, and clinical photographs of the optic nerves. Right macula-sparing homonymous hemianopia juxtaposed to an inferior arcuate glaucomatous type defect in the right eye and to a possible left-inferior quadrantanopia. RNFL quadrants with superior reduced thickness in both eyes. RNFL analysis thinning in the superior-temporal RNFL outside of normal limits in both eyes. Optic nerve photographs compatible with cupped glaucomatous disc. OCT, optical coherence tomography; RNFL, retinal nerve fiber layer.A Montreal Cognitive Assessment (MoCA) test showed a score of 25/30. Motor neurological examination showed a strength of 5−/5 except in the right upper limb that was 5/5 and in bilateral hip flexors 4+/5. Muscle tone was slightly increased bilaterally, predominantly in the left side. He had a slight intermittent left hand postural tremor, but no other resting tremor or abnormal movements. Sensation was reduced to pinprick, light touch, proprioception, and vibration in both feet. The rapid alternating movements' examination was slight slower in the left side. He walked with a wide-based gait and was not able to perform tandem walking. Posture was stable to the Pull Test, but Romberg was positive. MRI of the brain and orbits with and without contrast showed pachymeningeal and leptomeningeal enhancement in the bilateral parietal occipital region with extensive vasogenic edema (Fig. 1B). A positron emission tomography–computed tomography of the brain and whole body was performed which showed diffuse meningeal hypermetabolism consistent with the cranial MRI contrast enhancement. The patient's health status continued to deteriorate having a greater than 30-pound weight loss over a period of 2 months. A chest radiograph showed an old, inactive appearing, 8-mm-diameter calcified granuloma in the medial aspect of the right upper lung and a 9-mm-diameter calcified granuloma left lung apex. Serum interferon gamma release assay (T-spot) was positive. A right parietal subdural-pia-brain biopsy showed necrotizing granulomatous inflammation (Fig. 3). Seven weeks after the biopsy, the tissue culture grew Mycobacterium tuberculosis (MTB) sensitive to all 4 anti-TB drugs tested. The patient's systemic symptoms, signs, and MRI improved after initiation of anti-TB treatment with rifampin, isoniazid, pyrazinamide, and ethambutol.FIG. 3.: Histopathologic findings of the leptomeningeal/brain biopsy. A. Low power view shows brain parenchyma (B) and meninges (M) with a central inflammatory lesion with areas of necrosis (N) (hematoxylin and eosin). B. Edge of caseating necrosis (N) shows multinucleated giant cells, Langhans' type and a mantle of lymphocytes and epithelioid hystiocytes consistent with necrotizing granulomatous inflammation (hematoxylin and eosin).DISCUSSION Neuro-ophthalmologic manifestations of TB in order of frequency include papillitis, neuroretinitis, optic nerve tubercle, and granulomatous uveitis (3). A homonymous hemianopsia is a distinctly unusual presenting sign of TB (4,5). In their study, Davis et al reported that more than two-thirds of patients presenting with tuberculous optic neuropathy had resided in or traveled to an area endemic for TB, and visual field defects were reported for 46.8% of the patients' eyes (3). Central nervous system (CNS) TB can present as meningitis, intracranial tuberculoma, or spinal tuberculous arachnoiditis. TB can hematogenously spread to the CNS (6). LP may show elevated CSF protein, CSF lymphocytic pleocytosis, or low CSF glucose (7). Patients may experience vision loss from the disease or during antitubercular therapy either due to drug-induced optic neuropathy (ethambutol toxicity) or from paradoxical growth of a cerebral tuberculoma from an exaggerated immune response, worsening hydrocephalus, or inflammatory arachnoiditis (8). Table 1 shows all the previously reported case of CNS TB producing a juxtaposed homonymous hemianopsia. To the best of our knowledge, this is the first such case in a non-HIV/AIDS patient in the English language ophthalmic literature (4,5). TB (such as syphilis) remains the great mimicker of neuro-ophthalmic disease. It can present with acute or chronic presentations or a combination of acute on chronic disease (9,10). Clinicians should maintain a high suspicion for TB in any unexplained neuro-ophthalmic finding (including homonymous hemianopsia) especially in patients from endemic areas. TABLE 1. - Previously reported cases of homonymous hemianopsia in TB Author, Year City, Country Language # of Patients Sex and Age Main Finding Clinical Presentation Brain Imaging Type, Finding Outcome Sugiyama et al, 20054 Bunkyo-ku, Tokyo Japanese 1 Female, 53 Incidental finding of right incongruous homonymous quadrantanopia History of tuberculous meningitis at 3 y. o. MRI, left optic tract obscured by suprasellar calcified lesion No change Gharai et al, 20125 New Delhi, India English 1 Male, 30 Left-sided incongruous homonymous hemianopsia in newly diagnosed HIV/AIDS patient Sudden loss of vision in his left visual field. MRI, irregular lobulated lesion in the right temporo-occipital cerebral hemisphere and left high frontoparietal cerebral hemisphere Diagnosis of primary cerebral tubercular abscess. Four weeks after TB treatment, patient constitutional symptoms improved. Vision was never recovered. TB, tuberculosis. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: L. Wheelock-Gutierrez and S. H. Bindiganavile; b. Acquisition of data: L. Wheelock-Gutierrez and S. H. Bindiganavile; c. Analysis and interpretation of data: L. Wheelock-Gutierrez, S. H. Bindiganavile, and A. G. Lee. Category 2: a. Drafting the manuscript: L. Wheelock-Gutierrez, S. H. Bindiganavile, P. Chévez-Barrios, G. N. Fuller, N. Bhat, and A. G. Lee; b. Revising it for intellectual content: L. Wheelock-Gutierrez, S. H. Bindiganavile, P. Chévez-Barrios, G. N. Fuller, and A. G. Lee. Category 3: a. Final approval of the completed manuscript: L. Wheelock-Gutierrez, S. H. Bindiganavile, P. Chévez-Barrios, G. N. Fuller, N. Bhat, and A. G. Lee.

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