Papers of the Week

Posterior reversible encephalopathy syndrome encompasses a spectrum of disorders with a constellation of clinical symptoms and neuroradiological features. It is commonly encountered in organ transplant where it poses a challenge in the diagnosis and treatment in the absence of strong evidence. The underlying pathophysiology of posterior reversible encephalopathy syndrome is the loss of cerebral autoregulation following elevated blood pressure and/or endothelial dysfunction. It is more likely to happen in patients treated with cyclosporine versus with tacrolimus. Posterior reversible encephalopathy syndrome manifests as headache, visual disturbances, seizure, and abnormal mentation. The characteristic radiological features are the result of posterior- circulation vasogenic edema secondary to blood-brain barrier disruption. Treatment varies based on the etiology of the condition. In addition to the symptomatic management of hypertension and seizure disorders, switching or replacing the calcineurin inhibitor with another immunosuppressant or decreasing the dose of the calcineurin inhibitor is the key in calcineurin inhibitor-associated posterior reversible encephalopathy syndrome. Here, we have reviewed the terminology, pathogenesis, clinical features, diagnosis, and treatment of posterior reversible encephalopathy syndrome with special reference to its presence in the posttransplant period.