MR Imaging Findings of Cortical Blindness Following Cerebral Angiography: Is This Entity Related to Posterior Reversible Leukoencephalopathy?

We read with interest Saigal et al’s (1) article, MR Findings of Cortical Blindness Following Cerebral Angiography, in the February 2004 issue of the AJNR. The authors reported MR imaging findings in three cases of cortical blindness following cerebral angiography in which nonionic contrast media were used. These cases exhibited clinical and radiological findings that were relatively similar to those associated with posterior reversible leukoencephalopathy (PRLE), which suggests a common pathophysiology. On the basis of their experience, Saigal et al have hypothesized that the pathophysiological mechanisms of cortical blindness following cerebral angiography and PRLE may be related.

Posterior reversible encephalopathy syndrome, hypertensive encephalopathy, reversible posterior cerebral edema syndrome, and PRLE are all terms that have been used to describe a group of disorders that present clinically with headache, seizures, visual changes, altered mental status, and occasionally, focal neurologic signs (1). CT and MR imaging of patients with these disorders typically show symmetrically distributed areas of vasogenic edema predominantly within the territories of the posterior circulation (2–5). The abnormalities affect primarily the white matter, but the cortex is also involved. Localized mass effect and subtle enhancement within the lesions have been described, but are not seen consistently.

Endothelial cell damage is believed to be the central pathophysiology of posterior reversible leukoencephalopathy syndrome (2–5). Although reversible vasogenic edema due to cerebrovascular autoregulatory dysfunction is the underlying pathophysiological mechanism, irreversible lesions resulting from cytotoxic edema can be found, especially in patients with seizure (2–5). Diffusion-weighted (DW) imaging is useful to distinguish between reversible vasogenic edema and cytotoxic edema resulting in ischemic injury. It stands to reason that DW imaging could be used to distinguish PRLE from other disease entities or to monitor for ischemia as a complication of PRLE. DW imaging studies of PRLE have showed that apparent diffusion coefficient (ADC) values in areas of abnormal T2 signal intensity were high (2–5). In addition, low ADC values compatible with cytotoxic edema may be found, especially in severe irreversible lesions resulting from cytotoxic edema in patients with seizure (2–5).

We have reviewed all of the images presented by Saigal et al (1) and found no abnormalities on the DW images or the ADC maps. In their article, the authors state the following: “The absence of evidence of restricted fluid motion on the diffusion-weighted images in all cases seems to be an important finding” (Vol. 25, No. 2, p. 225). The authors did not address the issue of ADC values in the case report section.

As further evidence of the correlation between the pathophysiology affecting the patients in their series and that of PRLE, Saigal et al have noted the gyriform hyperintensities in the occipital cortices that appear on all fluid-attenuated inversion recovery and T2-weighted MR images in their series. Although PRLE is associated with cortical involvement, its effects are normally confined to subcortical white matter. Cortical involvement without subcortical white matter involvement is not normally associated with PRLE.

Because the ADC map and DW imaging findings and the cortical involvement patterns of cases presented by Saigal et al (1) are dissimilar to those associated with PRLE, we believe that the pathophysiological mechanisms of cortical blindness following cerebral angiography and PRLE are probably not related.

The true biochemical mechanisms of cerebral injury remains speculative in patients with cortical blindness following cerebral angiography. The incidence of transient cortical blindness is reported to range from 0.3–1% when nonionic contrast agents are used, but it can be as high as 4% when hyperosmolar iodinated contrast agents are used (6). Transient cortical blindness was reported in cerebral, vertebral, brachial, aortic arch, renal, and coronary angiography, translumbal aortography, and myelography (6). The highest incidence was reported following vertebral angiography (6). The highest incidence of cortical blindness following vertebral angiography and the higher risk of cortical blindness with nonionic contrast agent use makes us think that the possible explanation is a direct neurotoxicity of the contrast agent itself to sensitive occipital cerebral lobes.