Snapshot A 66-year-old man presents to the emergency department after being found down in a park. He is accompanied by a person who witnessed the fall, who said he had seizure-like activity prior to falling on the floor. The patient is non-participatory on exam but is able to breath on his own. Laboratory studies is significant for a serum sodium of 117 mEq/L. Over the course of 6 hours, his serum sodium was corrected to 135 mEq/L. Subsequently, in the next few days he develops quadrapresis with preservation of eye blinking. Introduction Definition neurological sequelae from rapid fluctuations in brain osmolality Epidemiology Risk factors chronic hypernatremia rapid sodium correction (> 8-10 mEq/day) Pathogenesis Normally, the brain has adaptive mechanisms to prevent swelling in hypotonic states recall that hypotonicity in the serum favors movement of water into cells As the body increases in sodium, it pulls the water out of neurons, dehydrating them, and causing demyelination also causes astrocytic cell death Presentation Symptoms/physical exam can lead to a range of symptoms asymptomatic seizures loss of conciousness dysarthria and dysphagia locked-in syndrome muscle paralysis with sparing of eye blinking Imaging MRI brain indication patients with nonspecific neurological findings after rapid sodium correction findings noninflammatory myelinolysis Differential Wernicke encephalopathy differentiating factor gait ataxia oculomotor dysfunction encephalopathy Treatment Preventative slow sodium correction indication slowly correct sodium 6-8 mEq/L per day in patients with chronic hyponatremia there is no effective treatment for ODS Complications Locked-in syndrome Death