Journal of Clinical Practice · Published 2026-06-18 · DOI 10.17816/clinpract705153
Elena V. Shirshova, Irina V. Zakharchuk, Elena O. Kontarova, Alexander V. Lugovoy, Matthew O. Shkap, Vladimir P. Baklaushev
BACKGROUND: Osmotic demyelination syndrome is an acutely developing, localized, symmetrical, non-inflammatory demyelination in the middle portion of the basis pontis (central pontine myelinolysis, CPM) or in the white matter of the cerebral hemispheres (extrapontine myelinolysis). Demyelination occurs in the most compactly arranged white matter as a result of cellular edema caused by an abrupt reversal of the osmotic gradient, the most common cause of which is rapid correction of chronic hyponatremia against a background of intracellular osmolyte depletion. The disease may also develop in association with other electrolyte and metabolic disturbances, including hypernatremia, hyper- or hypochloremia, hypokalemia, nutritional deficiency, intoxication, hyperglycemia, and hypertriglyceridemia, and may be a complication of diuretic or psychoactive drug use, hepatic and renal failure, and other conditions. Before the neuroimaging era, the disease was considered rare and was detected only at autopsy; however, after the introduction of MRI, it became evident that this syndrome is a relatively common complication in intensive care patients and may account for 0.23–2.5% of all cases of water–electrolyte disturbances, including asymptomatic or oligosymptomatic forms. CLINICAL CASE DESCRIPTION: We present a clinical case of CPM in a young female patient born in 1987 who, after an episode of severe nutritional disturbances leading to hyponatremia and its subsequent correction, developed pseudobulbar syndrome, tetraparesis, and ataxia. The diagnosis was confirmed by reconstruction of blood sodium dynamics from the discharge summary, which demonstrated excessively rapid correction of hyponatremia (initial hyponatremia 101.8 mmol/L; after 24 hours: 121 mmol/L; after 48 hours: 135.5 mmol/L), as well as by brain MRI findings showing a characteristic trident-shaped lesion in the central pons. Following treatment and rehabilitation, a significant regression of the neurological deficit was achieved, with complete functional recovery. CONCLUSION: This case demonstrates the importance for intensive care physicians and related specialists of recognizing the high risk of osmotic demyelination during rapid correction of water–electrolyte disturbances and of implementing timely prevention of this severe complication in accordance with current clinical guidelines.
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Shirshova, E., Zakharchuk, I., Kontarova, E., et al. (2026). CENTRAL PONTINE MYELINOLYSIS: A NEW PERSPECTIVE ON ITS PREVALENCE AND PREVENTION. Journal of Clinical Practice. https://doi.org/10.17816/clinpract705153