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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.

Introduction: Glymphatic fluid circulation may be considered the lymphatic system of the brain and the main role of such system seems to be played by aquaporins (AQPs), a family of proteins which regulates water exchange, in particular AQP4 and 1. Alterations of glymphatic fluid circulation through AQPs variations are now emerging as central elements in the pathophysiology of different brain conditions, like hydrocephalus. This systematic review provides an insight about the role of AQPs in hydrocephalus establishment and compensation, investigating their possible role as diagnostic tools or therapeutic targets. Methods: PubMed database was screened searching for the relevant existing literature in English language published until February 29th 2020, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Statement. Results: A total of 40 articles met the inclusion criteria for our systematic analysis. AQP4 resulted the most studied water channel, followed by AQP1. The changes in cerebrospinal fluid (CSF), brain parenchyma and choroid plexus (CP) in different hydrocephalus type were analyzed. Moreover, important pharmacological interactions regarding AQP and molecules or conditions were discussed. A very interesting result is the general consensus on increase of AQP4 in hydrocephalic patients, unless in patients suffering from idiopathic normal pressure hydrocephalus, where AQP4 shows a tendency in reduction. Conclusion: AQP seem to play a central role in the pathophysiology of hydrocephalus and in its compensation mechanisms. Further studies are required to definitively establish their precise roles and their quantitative changes to allow their utilization as diagnostic tools or therapeutic targets.