A 38-year-old woman with uncontrolled type 1 diabetes (HbA1c 12.8%) was admitted for diabetic ketoacidosis (731 mg/dL blood glucose). Hyperglycemia was corrected within 24 hours to 129 mg/dL. Upon presentation, her sodium and potassium levels were 139 and 3.9 mmol/L, respectively, remaining stable until discharge. There was no history of malnutrition or alcohol abuse.
Four days later, the patient developed acute diffuse pyramidal weakness. Brain MRI revealed symmetric restricted diffusion in the pons with normal magnetic resonance angiography (figure). The patient remained stable and was discharged to a rehabilitation facility.
T2 fluid-attenuated inversion recovery (FLAIR) reveals symmetric hyperintensities centered in the pons (A) with restricted diffusion (B). T1 postcontrast with gadolinium demonstrated no enhancement (C). DWI = diffusion-weighted imaging; GAD = gadolinium.
Central pontine myelinolysis (CPM) is a clinically heterogeneous neurologic disorder of demyelination in the pons, usually from rapid correction of hyponatremia.1,2
Diabetic ketoacidosis is an uncommon cause of CPM with uncertain physiopathology.3 Here, it is plausible that a rapid drop in osmolality in a chronic state of high osmolality (uncontrolled diabetes) led to CPM. A slower correction of hyperglycemia possibly could have prevented it.
Study Funding
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Footnotes
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Teaching slides links.lww.com/WNL/B447
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