Posterior Reversible Encephalopathy Syndrome Due to Hypocalcemia: A Very Rare Clinical Association
Bhargava Talluri1, Sandhya Manorenj2*,Sara Sravan Kumar3
1Neurology Resident, Department of Neurology, Princess Esra Hospital, Deccan College of Medical sciences, Hyderabad, Telangana, India.
2Senior Consultant Neurology, KIMSHEALTH Trivandrum and Former Professor & Head, Department of Neurology, Princess Esra Hospital, Deccan College of Medical sciences, Hyderabad, Telangana, India.
3Assistant Professor Neurology,Department of Neurology, Princess Esra Hospital, Deccan College of Medical sciences, Hyderabad, Telangana, India.
*Corresponding Author: Sandhya Manorenj, Senior Consultant Neurology, KIMSHEALTH Trivandrum and Former Professor & Head, Department of Neurology, Princess Esra Hospital, Deccan College of Medical sciences, Hyderabad, Telangana, India.
DOI: https://doi.org/10.58624/SVOANE.2026.07.013
Received: April 24, 2026
Published: May 11, 2026
Citation: Talluri B, Manorenj S, Kumar SS. Posterior Reversible Encephalopathy Syndrome Due to Hypocalcemia: A Very Rare Clinical Association. SVOA Neurology 2026, 7:3, 80-85. doi.org/10.58624/SVOANE.2026.07.013
Abstract
Introduction: Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiographic neurovascular disorder. Recognized risk factors for PRES include hypertension, renal disease, autoimmune disorders, preeclampsia, sepsis, and exposure to cytotoxic or immunosuppressive therapies. Hypomagnesemia and hypercalcemia, are very rarely associated with PRES. Here, we report three patients with severe hypocalcemia that presented with PRES syndrome that improved with calcium replacement.
Case Summary: In this prospective case series, we describe the clinical, biochemical, and radiological characteristics of PRES associated with hypocalcemia in the absence of classical risk factors. Three patients presented with PRES with significant hypocalcemia secondary to vitamin D deficiency. All cases demonstrated favorable clinical outcomes following standard management of PRES along with correction of the underlying hypocalcemia.
Conclusion: The study identifies hypocalcemia as a potential cause for PRES. It further expands existing literature of hypocalcemia as a rare contributory risk factor. Key Message: Hypocalcemia is a novel and important, treatable metabolic cause of PRES that should be looked in during evaluation of PRES.
Keywords: Hypocalcemia, PRES, Seizures, Encephalopathy.
