Clinical Insights into Osmotic Demyelination Syndrome: Two Case Studies

Osmotic demyelination syndrome (ODS) is a critical neurological condition characterized by acute non-inflammatory demyelination of central nervous system structures, primarily resulting from rapid correction of chronic hyponatremia. This article presents a detailed examination of two distinct cases of ODS, providing insights into their clinical presentations, diagnostic challenges, and therapeutic implications.

ODS typically arises when sodium levels in the blood are corrected too quickly, leading to cellular dehydration and subsequent neurological impairment. The cases discussed in this article underscore the necessity for vigilant monitoring of electrolyte levels and the gradual correction of sodium concentrations, especially in high-risk patients.

**Case Details**

**Case 1:** A 67-year-old male patient was admitted to a neurological intensive care unit exhibiting symptoms of acute confusion, left-sided weakness, and dysphagia following a bout of gastroenteritis characterized by prolonged diarrhea and vomiting. Upon hospitalization, he received aggressive rehydration and electrolyte replacement. Approximately 72 hours post-correction, the patient exhibited classic extrapyramidal signs consistent with ODS, including severe dysarthria and rigidity. Neuroimaging with MRI revealed symmetric hyperintensities in the pons and basal ganglia, characteristic of ODS (Elimam et al., 2025).

**Case 2:** A 51-year-old male patient presented with atypical ODS symptoms, including diplopia and facial asymmetry, following self-administered fluid replacement amidst alcohol abuse. Despite normal serum sodium levels, the MRI scan showed diffuse hyperintensities in the pons and cerebellar regions—findings not commonly associated with ODS (Elimam et al., 2025). His diagnosis was complicated by the presence of both neurological symptoms and atypical imaging findings, necessitating careful clinical correlation.

**Clinical Implications**

Both cases illustrate the phenotypic diversity of ODS, with one patient exhibiting classic features linked to rapid sodium correction and the other displaying atypical manifestations despite normal sodium levels. These findings align with the broader literature indicating that ODS can occur in individuals with normonatremia and highlight the need for enhanced diagnostic vigilance among clinicians (Danyalian & Heller, 2024; Bansal & Zinkus, 2019).

The pathophysiological mechanisms underlying ODS involve astrocyte dysfunction triggered by rapid shifts in serum osmolality. This dysfunction can lead to the release of inflammatory mediators and consequent demyelination, even in the absence of severe electrolyte imbalances (Kilinc et al., 2002; Lohr, 1994).

**Preventive Strategies**

To mitigate the risk of ODS, clinical guidelines recommend a cautious approach to sodium correction, restricting increases to 6–9 mmol/L over a 24-hour period. In cases of severe hyponatremia (serum sodium <120 mmol/L), administration of hypertonic saline should be considered, ideally in conjunction with desmopressin to reduce the risk of overcorrection (Achinger & Ayus, 2019).

**Conclusion**

Osmotic demyelination syndrome remains a significant clinical challenge, particularly given its variable presentations and potential for severe neurological impairment. By acknowledging the potential for atypical presentations and implementing careful monitoring protocols, healthcare providers can improve outcomes for patients at risk of this complex syndrome. As the understanding of ODS evolves, ongoing research into its pathogenesis and treatment strategies will be crucial for advancing clinical practice.

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