As the fibers course through the retrochiasmal visual pathway (which consists of the optic tract; lateral geniculate body; and temporal, parietal, and occipital lobe visual radiations), crossed nasal fibers from the contralateral eye and uncrossed temporal fibers from the ipsilateral eye come together (see Chapter 1). Retrochiasmal damage results in homonymous visual field defects that continue to respect the vertical midline. As fibers progress from the anterior to the posterior visual pathway, those from corresponding retinal regions of each eye tend to run more and more closely together. Lesions of the optic radiations classically produce dissimilar (incongruous) defects in the corresponding homonymous hemifields, whereas more posterior damage results in progressively similar (congruous) defects as lesions approach the occipital lobes. Although a highly congruous homonymous hemianopia might be expected to reflect occipital disease, the possibility of a more anterior lesion involving the optic tract or the lateral geniculate body cannot be excluded. Lesions severe enough to produce complete hemianopic defects may occur at any anteroposterior retrochiasmal location; such defects do not help localize lesions from the chiasm through the occipital cortex. Stroke is the most common cause of homonymous hemianopias, followed by traumatic brain injury and tumor.
Kedar S, Zhang X, Lynn MJ, Newman NJ, Biousse V. Congruency in homonymous hemianopia. Am J Ophthalmol. 2007;143(5):772–780.
Zhang X, Kedar S, Lynn MJ, Newman NJ, Biousse V. Homonymous hemianopias: clinicalanatomic correlations in 904 cases. Neurology. 2006;66(6):906–910.
Lesions of the optic tract cause homonymous defects in the hemifields contralateral to the affected optic tract (see Fig 4-25). Damage to the optic tract frequently results from mass lesions such as aneurysms or tumors. These lesions may be associated with an ipsilateral RAPD if the optic nerve is also involved. Inflammatory and demyelinating lesions occasionally occur. Ischemic lesions of the tract are uncommon and result from infarction in the territory of the anterior choroidal artery. Because the fibers involved are primary neurons in the visual pathway (ie, retinal ganglion cells), the homonymous hemianopic visual field loss is accompanied by other findings that make up the optic tract syndrome:
“Bow-tie” optic atrophy. Because the optic tract involves crossed fibers from the contralateral eye, the corresponding atrophy of crossed retinal fibers (those nasal to the macula) involves the papillomacular fibers and the nasal radiating fibers in the contralateral eye, causing atrophy in the corresponding nasal and temporal horizontal portions of the ONH (known as band or bow-tie atrophy) (see Chapter 1, Fig 1-18). Atrophy in the ipsilateral eye involves only the arcuate temporal bundles, which enter the ONH at the superior and inferior poles.
Mild RAPD in the contralateral eye. This finding stems from the presence of greater sensitivity of the nasal retina than the temporal retina and the presence of more crossed than uncrossed pupillary fibers in the tract, causing more pupillary fibers from the contralateral eye to be damaged by a tract lesion.
Kardon R, Kawasaki A, Miller NR. Origin of the relative afferent pupillary defect in optic tract lesions. Ophthalmology. 2006;113(8):1345–1353.
Savino PJ, Paris M, Schatz NJ, Orr LS, Corbett JJ. Optic tract syndrome. A review of 21 patients. Arch Ophthalmol. 1978;96(4):656–663.
Excerpted from BCSC 2020-2021 series: Section 5 - Neuro-Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.