A 60-year-old man with a known history of abdominal aortic aneurysm (AAA) with associated thrombus, who had been lost to follow-up, presented with visual loss 2 months after experiencing a stroke. His stroke occurred in the setting of a ruptured AAA, which led to cardiac arrest with pulseless electrical activity lasting 12 minutes before return of spontaneous circulation after cardiopulmonary resuscitation.

The patient reported blurred vision in both eyes. Humphrey visual fields (24–2) demonstrated the rarely reported crossed-quadrant homonymous hemianopia, also known as “checkerboard visual field loss” (CVFL) (Figure 1A, 1B). The neurological exam was otherwise unremarkable except for intermittent non-pulsatile tinnitus. Stroke workup included brain MRI, which revealed infarcts in the right inferior temporal-occipital (Figure 1C) and left occipital lobes (Figure 1D). A standard diagnostic evaluation was undertaken to investigate potential etiologies of his stroke, including cardiac and vascular sources of embolism, as well as rhythm monitoring for occult arrhythmia. Despite the comprehensive workup, no definitive cause of stroke was identified, and the etiology was presumed to be multifactorial, involving hypoperfusion related to prolonged cardiac arrest and/or a possible embolic component related to the ruptured AAA.

Figure 1.

Humphrey’s visual field 2 months after stroke reveals a crossed-quadrant homonymous hemianopsia (A,B). T2-weighted Fluid-Attenuated Inversion Recovery sequence reveals stroke in the right inferior temporal-occipital (C) and left occipital regions (D).

In this patient, a right inferior temporal-occipital infarction produced a left superior quadrantanopia, while a left occipital infarction caused a right inferior homonymous hemianopia. Despite multiple end-organ damages, there were no other strokes. As the posterior cerebral artery (PCA) territory does not inherently demonstrate an increased predilection for embolic insults originating from a central source, the exclusive occurrence of strokes within the PCA territory in this patient remains unexplained.

First described in 1990, CVFL is a rare pattern of visual loss that has been seldom reported in the literature and is most often seen in the context of bilateral infarction of the calcarine arteries.^{Reference Dyer, Hirst, Vandeleur, Carey and Mann1,Reference Kamal, Al Othman, Kini and Lee2} CVFL can alternatively represent bilateral simultaneous or sequential post-chiasmal lesions of other causes, including demyelination, inflammation or trauma.^{Reference Kamal, Al Othman, Kini and Lee2} The etiology of documented causes includes cerebrovascular accidents, multiple sclerosis, syphilis and necrotizing ependymomyelitis.^{Reference Kamal, Al Othman, Kini and Lee2,Reference Cesareo, Pozzilli, Ristori, Roscioni and Missiroli3,Reference Cross and Smith4,Reference Tamhankar, Markowitz and Galetta5} While the visual field loss was not detected in this case prior to formal perimetry, CVFL can be clinically elicited via careful confrontation visual field testing. The sensitivity of confrontation visual field assessment improves when a colored stimulus, that is, red cotton ball or red cap, is used.