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Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
Published on: November 8, 2018
[Hypomagnesemia and Wernicke's encephalopathy]
Julio César Rotondaro1, Ignacio Saguier Padilla2, Magalí Gutiérrez1
1Unidad de Cuidados Especiales, Sanatorio Mater Dei, Buenos Aires, Argentina.
Abstract:
A 74-year-old male with a history of problematic alcohol use, laxative and proton pump inhibitor consumption, presented with acute behavioral changes, tremors, gait disturbance, nystagmus, and tonic-clonic seizures associated with fever. A lumbar puncture was performed, showing no physicochemical abnormalities, no growth in cultures, and a negative polymerase chain reaction panel for common pathogens. Laboratory tests revealed severe hypomagnesemia, hypokalemia, hypocalcemia, and metabolic alkalosis. Neuropsychiatric symptoms and the acute symptomatic seizure were interpreted as secondary to electrolyte disturbances, mainly hypomagnesemia. Since Wernicke's encephalopathy could not be ruled out as a concurrent cause. Thiamine was administered along with aggressive electrolyte replacement, leading to reversal of the clinical picture. Neuropsychiatric manifestations in patients with hypomagnesemia are uncommon and often underdiagnosed or underestimated. Although an association between Wernicke's encephalopathy and hypomagnesemia has been described, there is no strong evidence regarding the interaction of both processes and their consequences. It is known that failure to correct magnesium perpetuates or makes Wernicke's encephalopathy refractory to thiamine administration.
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