Neuro-ophthalmic manifestations of tuberculosis

Abstract

Neuro-ophthalmic features are a known association in tuberculosis, especially common in central nervous system tuberculosis (CNS-TB). They are mostly the result of the visual pathway and/or ocular motor and other cranial nerve involvement. Furthermore, toxic optic neuropathy and paradoxical response to anti-tubercular drugs (ATT) are also not uncommon. The etiopathogenesis is by the complex interplay of various factors like exudates, vasculitis, arachnoiditis, presence of tuberculomas, hydrocephalus, brain infarcts and/or immune-mediated reaction. The entity often poses a diagnostic dilemma for the ophthalmologists/neuro-ophthalmologists and may lead to irreversible vision loss. The presence of neuro-ophthalmic features not only affect the visual outcome but are also predictors of systemic morbidity of the disease. Therefore, understanding and knowledge about this entity are necessary for the comprehensive management of the disease. While various forms of TB including CNS-TB have been well-dealt with in literature, little is discussed specifically about the neuro-ophthalmic manifestations of tuberculosis. Therefore, the purpose of this review is to highlight current understanding of the types of neuro-ophthalmic involvement in tuberculosis, its etiopathogenesis, diagnosis and management.

Fig. 1. Radiological features of tuberculous meningitis.

A Basal exudates: axial post gadolinium T1-weighted image showing smooth thin enhancement of the prepontine cistern (arrow). The enhancement is also seen along the cerebellar sulci (dashed arrow); B basal exudates: sagittal post gadolinium T1-weighted image showing smooth enhancement of the basal cisterns (arrows). Enhancement is also seen along the cerebellar sulci (dashed arrow); C exuberant basal exudates: axial post gadolinium T1-weighted image showing nodular enhancement of the perimesencephalic cisterns (arrows) and mass effect on the optic chiasma (dashed arrow); D basal exudates with tuberculomas: axial post gadolinium T1-weighted image showing smooth thin enhancement of the perimesencephalic cisterns (arrow) and multiple ring-enhancing granulomas (dashed arrow).

Fig. 2. Radiological and ocular features in a patient with CNS tuberculoma and choroid tubercle.

A Suprachiasmatic tuberculomas: Axial post gadolinium T1-weighted image showing disc-like enhancing tuberculomas in the suprachiasmatic location (arrows) and causing mass effect on the optic chiasma (dashed arrow); B suprachiasmatic tuberculomas mimicking a mass: coronal post gadolinium T1-weighted image showing coalescent enhancing tuberculomas in the suprachiasmatic location (arrow) mimicking a mass causing compression of the underlying optic chiasma (dashed arrow). C Fundus picture of the right eye of the same patient showing choroidal tubercle in the supero-temporal macula (arrow). D The posterior segment OCT of the same eye showing a choroidal bump with a contact sign (arrow).

Fig. 3. Tuberculomas with central caseation in two different patients.

A Axial FLAIR image showing a tuberculoma in the midbrain with characteristic central hypointense signal (arrow) and extensive surrounding oedema involving the periaqueductal grey matter and expected location of the left oculomotor and Edinger–Westphal nucleus; B sagittal T2-weighted image showing a lesion with characteristic central T2 hypointensity (dashed arrow) with minimal surrounding oedema in the lateral occipital cortex. C Optochiasmatic arachnoiditis: axial post gadolinium T1-weighted image showing smooth thin enhancement along the lining of optic chiasma and bilateral optic nerves (arrow). The enhancement is also seen along with the basal cisterns (dashed arrow). D Typical findings of TB: coronal post gadolinium T1-weighted image showing smooth thin enhancement of the basal cisterns (arrow) with hydrocephalus (asterisk) and gyriform enhancement along the right temporal lobe (dashed arrow, secondary to a subacute infarct).

Fig. 4. Magnetic resonance spectroscopy of a tuberculoma.

Spectrum from a single-voxel spectroscopy showing a decreased N-acetyl aspartate peak (NAA) at 2.0 ppm and a characteristic high lipid peak (lip) at 0.9–1.3 ppm.