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    Central Pontine Myelinolysis Medical Slides

    Generate publication-quality central pontine myelinolysis lecture slides in 30 seconds. AI-powered content structured for clinical education.

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    Why teach Central Pontine Myelinolysis?

    Osmotic demyelination syndrome (ODS), including central pontine myelinolysis (CPM) and extrapontine myelinolysis, results from rapid correction of chronic hyponatremia, causing non-inflammatory demyelination of the pons and other vulnerable brain regions. The condition is preventable with adherence to sodium correction limits of ≤8-10 mEq/L per 24 hours. Teaching ODS integrates the pathophysiology of osmotic stress, safe sodium correction protocols, and recognition of delayed neurological deterioration.

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    01Pathophysiology: Organic Osmolyte Depletion, Rapid Osmotic Shift, and Oligodendrocyte Vulnerability
    02Risk Factors: Chronic Hyponatremia, Alcoholism, Malnutrition, Liver Transplantation, and Hypokalemia
    03Safe Sodium Correction: The ≤8 mEq/L/24h Rule and Risk-Adapted Targets
    04Clinical Presentation: Biphasic Course — Initial Improvement Then Neurological Deterioration
    05MRI Diagnosis: Pontine Trident Sign on T2/FLAIR and DWI (Delayed Appearance at 2-4 Weeks)
    06Treatment: DDAVP Rescue Protocol for Overcorrection, Supportive Care, and Outcomes
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    Central Pontine Myelinolysis Presentation FAQ

    How should the safe sodium correction protocol be presented?

    Emphasize the prevention-focused approach: correct sodium by ≤8 mEq/L in 24 hours (some guidelines allow ≤10 in low-risk, but ≤6 in high-risk patients — alcoholism, malnutrition, hypokalemia, Na <105). Teach frequent monitoring: serum sodium every 2-4 hours initially. If overcorrection occurs (>10 mEq/L), immediately administer DDAVP 2-4 mcg IV + D5W to re-lower sodium back to the safe range ("re-lowering protocol"). This rescue strategy can prevent ODS if applied within 24 hours of overcorrection.

    What is the typical clinical course and how should it be taught?

    Present the characteristic biphasic course: initial neurological improvement as hyponatremia corrects (days 1-3), followed by delayed deterioration at 2-7 days with dysarthria, dysphagia, quadriparesis, and "locked-in syndrome" in severe cases. Extrapontine involvement adds movement disorders (parkinsonism, dystonia, mutism). This biphasic pattern is the key teaching point — clinicians must maintain high suspicion even after initial clinical improvement and obtain MRI if delayed symptoms emerge.

    When does MRI become positive and how should the timing be taught?

    Emphasize the critical teaching point that MRI may be normal in the first 1-2 weeks despite clinical symptoms. T2/FLAIR shows the classic pontine "trident" or "bat-wing" hyperintensity, and DWI may show restricted diffusion earlier (within days). A normal MRI does not exclude ODS if obtained early — repeat imaging at 2-4 weeks is recommended if clinical suspicion persists. This prevents premature diagnostic reassurance based on early negative imaging.

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