Posterior reversible encephalopathy syndrome (PRES): A narrative review of pathophysiology, clinical insights, and advances in management

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) is an acute neurological condition characterized by a spectrum of clinical and radiological features. It is most often associated with severe hypertension, renal dysfunction, autoimmune disease, sepsis, and exposure to cytotoxic or immunosuppressive agents. Although increasingly recognized in emergency and critical care practice, its pathophysiology remains incompletely understood and diagnostic challenges frequently delay treatment. Reported mortality ranges from 10 to 19%, and up to 40–44% of patients experience persistent neurological deficits or residual radiologic lesions, highlighting its clinical relevance. MAIN BODY: The clinical manifestations of PRES range from seizures, headache, and visual disturbance to confusion and reduced consciousness. Seizures occur in as many as 60–90% of cases, particularly in younger populations. Magnetic resonance imaging is the diagnostic modality of choice, revealing characteristic vasogenic edema, most prominently in the posterior cerebral regions, although atypical patterns are frequently observed. Misdiagnosis remains common due to overlap with stroke, encephalitis, and other acute neurological syndromes. Management is primarily supportive and directed at controlling the underlying precipitant. Blood pressure stabilization, withdrawal or adjustment of offending agents, and short-term antiseizure therapy form the cornerstone of treatment. Although most patients show clinical and radiologic recovery within weeks, complications such as intracranial hemorrhage, infarction, or recurrent PRES may occur. Special populations including pediatric, obstetric, and transplant patients require tailored evaluation and management strategies due to distinct risk profiles. Emerging research highlights endothelial dysfunction, blood–brain barrier disruption, and immune-mediated injury as central mechanisms. Investigations into biomarkers, advanced neuroimaging techniques, and targeted therapeutic approaches are opening opportunities for earlier detection and improved outcomes. CONCLUSION: PRES is reversible in many cases yet remains a potentially life-threatening syndrome with substantial morbidity and mortality. Early recognition, systematic neuroimaging, and rapid correction of precipitating factors are essential to optimizing outcomes. Future advances will depend on deeper mechanistic insight, validation of prognostic biomarkers, and development of standardized, evidence-based management protocols to guide care across diverse patient populations.