Contrast-induced encephalopathy and permanent neurological deficit: A case report and literature review

Abstract

Background: Contrast-induced encephalopathy (CIE) is a rare condition that occurs after intravenous or intra-arterial contrast agent administration. Patients generally show different ranges of neurological deficits, which generally resolve themselves spontaneously within 24–48 h or in rare cases within 2 weeks. Case Description: We report a case of CIE in a 54-year-old woman during retreatment for recanalization of communicating anterior artery aneurysm and with no history of allergic reaction to contrast agent. After the procedure, the patient developed right hemiplegia and complete aphasia; an MRI performed at 6 days excluded any signs of new ischemia and revealed a hyperintense signal on FLAIR sequences in the left cortical precentral gyrus corresponding to a hyperintense signal on DWI, suggesting a vasogenic edema. After 6 months, she clinically improved even if her previous neurological status was never restored while radiological findings did not change. Conclusion: According to the literature, many risk factors may play a role in the pathogenesis of CIE: we hypothesized that, among all of them, chronic hypertension and previous cerebral ischemic lesions were the most important in our case. Further studies are necessary to find the correlation between possible risk factors and neurotoxicity.

Contrast-Induced Encephalopathy: A Clinical Conundrum

“…Transient cortical blindness is the most common manifestation [10]. The literature review indicated that symptoms of neurological dysfunction presented within minutes to hours after contrast agent administration, and most patients fully recovered within 48-72 hours with supportive management [7][8][9]. In our patient, the symptoms resolved completely within 48 hours, which was consistent with the clinical course of CIE. We suspect that the severity of symptoms in our patient was related to her advanced age, hypertension, and other risk factors, which may have increased blood-brain barrier permeability, resulting in neurotoxicity and CIE.…”

“…This supports the hypothesis that the symptoms are a result of the chemotoxic effect of hyperosmolar media resulting in microvascular sludging and arterial spasms, causing shrinkage of the endothelial cells and disruption of tight junctions. The accumulation of iodinated contrast has also been known to cause a localized neurotoxic effect on the blood-brain barrier by increasing the expression of endothelin, amplifying endothelial cell permeability, and resulting in cerebral edema [7][8][9]. However, in our case, the contrast was administered intravenously for a CTPE study.…”

“…IV steroids and mannitol have been used sporadically with favorable outcomes. In patients with renal insufficiency on dialysis who develop CIE, hemodialysis has proven beneficial [5,8,9,11].…”

“…The diagnosis of CIE requires a high index of suspicion, and brain imaging is usually pathognomonic showing contrast enhancement in the cortical, subarachnoid, striatal spaces, or cerebral edema, which are important for the differentiation of CIE from other pathologies such as thromboembolism and hemorrhage [ 8 , 9 , 11 ]. Typically, symptoms resolve within days and the disease runs a benign course, but cases of persistent neurological deficit and even fatal cerebral edema secondary to contrast injection have been reported.…”

Fully Reversible Contrast-Induced Encephalopathy Mimicking Stroke after Flow Diverter Treatment of Carotid Cave Aneurysm

“…4 Although mostly transient and reversible, the symptoms may be persistent with permanent sequelae and adverse clini-cal outcomes. 5 Herein, we report a case of CIE following flow diverter treatment that mimicked a severe anterior circulation stroke.…”