Visual loss due to optic chiasm and retrochiasmal visual pathway lesions

Abstract

Purpose of review: Building on the anatomic and diagnostic approaches presented elsewhere in this issue of CONTINUUM, this article presents important differential considerations for chiasmal and retrochiasmal vision loss, useful strategies for confirming the underlying etiology, principles of their natural history, and, where appropriate, treatment strategies.

Recent findings: Although a wide variety of pathologic processes can affect the optic chiasm and retrochiasmal visual pathways, those commonly seen in neurologic practice are comparatively fewer in number. This article updates current understanding of vision loss localizing to the optic chiasm, including pituitary adenoma, sellar meningiomas, and aneurysms. Important causes of retrochiasmal vision loss, including stroke and posterior reversible encephalopathy syndrome, are also presented.

Summary: The optic chiasm and retrochiasmal visual pathways are susceptible to various forms of injury, with resultant patterns of vision loss that can be precisely localized on the basis of clinical and neuroimaging findings. Accurate localization, in association with other clinical features, allows for consideration of relevant differential diagnoses, which can be confirmed through the judicious application of appropriate diagnostic studies. Accurate localization, diagnosis, and robust clinical surveillance are essential to the effective management and treatment of these causes of vision loss.

Figure 6-1.

Relationship of the chiasm to the sella (sagittal view). o.n. = optic nerve; c = optic chiasm; t = tuberculum sella; p = pituitary gland; d = dorsum sella. Reprinted with permission from Glisson CC, Continuum (Minneap Minn). © 2009 American Academy of Neurology. journals.lww.com/continuum/Fulltext/2009/08000/BILATERAL_VISUAL_LOSS_APPROACH,_LOCALIZATION,_AND.6.aspx.

Figure 6-2.

Humphrey visual field testing demonstrates a dense, bitemporal hemianopsia, with exquisite respect for the vertical meridian.

Figure 6-3.

MRI of the brain (with and without contrast) demonstrates a well-defined enhancing mass in the region of the sella turcica, measuring 3.5 cm × 2.5 cm × 2.5 cm, with suprasellar extension causing mass effect and superior displacement of the optic chiasm. A, a sagittal T1-weighted MRI without contrast; B, sagittal T1-weighted MRI with contrast; C, coronal T2-weighted image; D, coronal T1-weighted image with contrast; E, axial T1-weighted image with contrast.

Figure 6-4.

Enhanced T1-weighted coronal (A) and axial (B) MRI of the brain demonstrated a large pituitary tumor with ischemia (note the necrotic/hypointense center) and a ring of gadolinium enhancement (termed the pituitary ring sign). Reprinted with permission from Vaphiades MS, Medscape Reference. © 2014 Medscape Reference. emedicine.medscape.com/article/1198279-overview.

Figure 6-5.

MRI of two patients with suprasellar meningiomas. Coronal (A) and sagittal (B) noncontrast T1-weighted MRI of a large meningioma (large arrows), isointense to brain. Note the normal sella and pituitary gland (P) (small arrows) in proximity to the large meningioma. Sagittal (C) and coronal (D) contrast-enhanced T1-weighted MRI of a planum meningioma extending into the sella. Note the upward deflection of the chiasm (arrow in C) and extension to the cavernous sinus (arrows in D). Modified with permission from Glaser JS, Glisson CC. Lippincott Williams & Wilkins. © 2013 Lippincott Williams & Wilkins.

Figure 6-6.

Humphrey visual field analysis demonstrates a left superior quadrantanopsia.

Figure 6-7.

Area of infarction in the distribution of the right posterior cerebral artery as seen on axial T2-weighted (A) and diffusion-weighted (B) MRI.

Figure 6-8.

Axial brain fluid-attenuated inversion recovery (FLAIR) MRI demonstrates extensive, diffuse, hyperintense signal involving the occipital lobes bilaterally, which is consistent with posterior reversible encephalopathy syndrome (PRES). Courtesy of Michael Vaphiades, DO.