Cortical laminar necrosis (CLN) is defined as focal or diffuse necrosis of one or more cortical laminae. It has been associated with various pathological conditions, such as hypoxia, infarction, metabolic encephalopathy, drugs, and infections.

Herein, we report a 48-years-old female patient with hypertension. She admitted to the emergency clinic because of confusion, nausea, and vomiting. Her hypertension was treated with amlodipine that was switched to perindopril, indapamide, and amlodipine two weeks ago. On admission, her serum sodium level was 103 mmol/L, and the patient was intubated following a generalized convulsive seizure. She was transferred to the intensive care unit. Due to the encephalopathy, the patient’s hyponatremia was rapidly corrected, and her serum sodium level was 130 mmol/L at 12^th hour. Her seizure was successfully treated with levetiracetam. One month after admission, she was consulted due to her confused status. On her neurological examination, the patient was disoriented with normal cranial nerve examination. The patient did not have any motor deficits despite brisk deep tendon reflexes. She did not have any pathological reflexes, and she had mild truncal ataxia. Her brain MRI revealed diffuse CLN. Her cerebrospinal fluid examination was within normal limits. Her EEG showed diffuse slowing with paroxysmal theta waves. The patient’s serum anti-neural antibodies were negative. The laboratory tests for the differential diagnosis of CLN were within normal limits, which suggested that the rapid correction of hyponatremia as the sole cause of this condition.

Glial cells are more sensitive than neurons to osmotic stress that results in myelinolysis because of the rapid correction of hyponatremia. Therefore, only a limited number of cases with CLN due to osmotic demyelination were reported in the literature. The underlying mechanism of CLN needs to be further investigated.