Contrast Medium-Induced Transient Cortical Blindness: A Systematic Review of the Literature

To summarize identified risk factors, the most common clinical presentations, radiological and neurophysiological features, and proposed pathophysiological mechanisms of contrast medium-induced transient cortical blindness (TCB).

A systematic search of PubMed, Cochrane Central Register of Controlled Trials, and clinicaltrials.gov was performed. A total of 115 patients from 2 retrospective cohort studies, 10 case series, and 52 case reports were included.

The available evidence suggests that TCB can manifest after both invasive and noninvasive contrast-enhanced procedures. The pathophysiology of TCB is unclear; however, the primary mechanism suggested involves the direct neurotoxic effect of the contrast medium. Ionic, nonionic, hyperosmolar, isoosmolar, and even ethiodized oil have been implicated. Imaging findings are nonspecific, and absent in about half of patients. Onset is within 30 minutes in about half of patients and resolves within 1 day in about half of patients, but delayed onset after a day and delayed resolution after a week may occur. Higher contrast medium dosage and its injection solely into the posterior circulation were the only risk factors identified in association with TCB.

TCB is a rare, idiopathic, and typically self-limited condition associated with direct posterior cerebral neurotoxicity of iodinated contrast media, and appears to be dose-dependent.