Corticosteroids in posterior reversible encephalopathy syndrome: Friend or foe? A systematic review.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is a complex neurological disorder characterized by symptoms such as headaches, seizures, confusion, and visual disturbances. The pathophysiology of PRES involves endothelial dysfunction, disrupted cerebral autoregulation, and resulting vasogenic edema. Hypertension and other factors that alter cerebral autoregulation are critical in its development. Corticosteroids, widely used for their anti-inflammatory and immunosuppressive properties, play a controversial role in PRES.

AIM: To elucidate the dual role of corticosteroids in the context of PRES by critically evaluating the existing literature. Specifically, it seeks to assess the results of PRES induced by corticosteroid therapy and the efficacy and safety of corticosteroids in the treatment of PRES. By synthesizing case reports and series, this review aims to provide a comprehensive understanding of the mechanisms, clinical presentations, and management strategies associated with corticosteroid-related PRES.

METHODS: The review was carried out according to the PRISMA guidelines. The databases searched included Science Direct, PubMed, and Hinari. The search strategy encompassed terms related to corticosteroids and PRES. Studies were included if they were peer-reviewed articles examining corticosteroids in PRES, excluding non-English publications, reviews, and editorials. Data on patient demographics, clinical characteristics, imaging findings, corticosteroid regimens, and outcomes were extracted. The risk of bias was evaluated using the Joanna Briggs Institute tool for case reports.

RESULTS: A total of 56 cases of PRES (66.1% women, 33.9% men) potentially induced by corticosteroids and 14 cases in which corticosteroids were used to treat PRES were identified. Cases of PRES reportedly caused by corticosteroids showed a mean age of approximately 25.2 years, with seizures, headaches, hypertension, and visual disturbances being common clinical sequelae. Magnetic resonance findings typically revealed vasogenic edema in the bilateral parieto-occipital lobes. High-dose or prolonged corticosteroid therapy was a significant risk factor. On the contrary, in the treatment cases, corticosteroids were associated with positive outcomes, including resolution of vasogenic edema and stabilization of symptoms, particularly in patients with underlying inflammatory or autoimmune diseases.

CONCLUSION: Corticosteroids have a dual role in PRES, capable of both inducing and treating the condition. The current body of literature suggests that corticosteroids may play a greater role as a precipitating agent of PRES rather than treating. Corticosteroids may induce PRES through hypertension and subsequent increased cerebral blood flow and loss of autoregulation. Corticosteroids may aid in the management of PRES: (1) Enhancing endothelial stability; (2) Anti-inflammatory properties; and (3) Improving blood-brain barrier integrity. Mechanisms which may reduce or mitigate vasogenic edema formation.