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.
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Reply:
We appreciate Dr. Albayram’s and Dr. Ozer’s interest in our article on posterior reversible leukoencephalopathy (PRLE). The authors are correct in their comments about the findings of PRLE (paragraph 2 of their letter), which we did not elaborate on in our article. We did not comment on the apparent diffusion coefficient (ADC) values in this regard. ADC values are increased in cases of PRLE because of vasogenic edema. Cytotoxic edema may occur in some patients, in which case low ADC values would be seen.
We must, however, disagree with the comment about the biochemical mechanisms being speculative in patients with cortical blindness following cerebral angiography. Both experimental and clinical studies (1–5) have shown that contrast media (both ionic and nonionic) cause a disruption of the blood-brain barrier (BBB), with resultant leakage of the contrast media into the adjacent brain. It is this pathophysiological mechanism that explains the CT hyperattenuation seen in the occipital lobes following injection of contrast medium (5, 6). Disruption of the BBB leads to the vasogenic edema, which may progress to cytotoxic edema, as suggested in PRLE (7). Similarly, disruption of the BBB leads to extravasation of contrast medium, with resultant contrast medium-induced neurotoxicity to the more sensitive occipital lobes. Extravasation of contrast material has been seen in both the cortical and subcortical areas in the occipital lobes (5, 8).
The reason why the posterior circulation is more commonly affected has also been extensively studied. Many theories exist, but the commonly accepted one is the paucity of sympathetic innervation of the vertebrobasilar system when compared with that of the internal carotid artery system (6, 7). That would also explain the higher incidence of cortical blindness in vertebral angiography, as we suggest.
The exact mechanism of neurotoxicity of contrast agents once they gain access to the brain parenchyma is open to speculation. It is thought that the toxicity may be related to the ability of the contrast agent to affect the membranes of the neurons or glia or idiosyncratic reaction, hypoxia, or edema (9). Hypertension has clearly been shown to be a factor that increases susceptibility of the endothelial cells to damage, and thus, increases the risk of both cortical blindness following angiography and PRLE (9, 10).
With regard to the imaging findings, we agree with the comment that ADC values are increased in cases of PRLE because of vasogenic edema. In addition, cytotoxic edema may occur in some patients, in which case low ADC values are seen. On a retrospective review of the cases we presented, the ADC values were slightly increased in two (cases 2 and 3). Unfortunately, because of the loss of data, we could not measure the ADC values in case 3. Also, one of the cases showed involvement of the subcortical white matter (case 1), and there was questionable involvement of the subcortical white matter in another (case 2). In case 3, however, only cortical involvement was noted. It is possible to have exclusive cortical involvement with pseudonormalization of the ADC values in PRLE, as suggested by Covarubbias et al (11). Also, there have been only two reports of exclusive cortical involvement in hypertensive encephalopathy syndromes (12, 13).
A relationship between these two entities has also been suggested by other authors on the basis of a similar pathophysiological mechanism (6, 10, 14).
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