Tacrolimus-associated Pontine Demyelination in a Liver Transplant Recipient: A Case Discussion and Review of the Literature
Objective:
To describe a case of central pontine myelinolysis (CPM) occurring in a liver transplant recipient receiving tacrolimus without sodium shifts.
Background:
Central pontine demyelination syndrome, or central pontine myelinolysis (CPM), is an uncommon but potentially devastating complication often seen in liver transplant recipients. Although classically associated with rapid correction of hyponatremia, an increasing body of evidence from case reports and small case-based series implicate calcineurin inhibitors such as tacrolimus as independent contributors to brainstem demyelination based on temporal association and improvement after drug withdrawal. Proposed mechanisms include endothelial dysfunction, blood–brain barrier disruption, and direct oligodendrocyte toxicity. MRI brain typically shows symmetric T2/T2-FLAIR hyperintensities in the pons. Discontinuation of medication can lead to clinical and radiologic improvement, but outcomes are variable.
Results:
A 24-year-old female with severe alcohol use disorder was admitted with acute alcoholic hepatitis complicated by liver failure requiring allogeneic liver transplantation and initiation of tacrolimus immunotherapy. Her postoperative course was notable for progressive quadriplegia, impaired axial strength, and sensory loss with preserved awareness. Head CT demonstrated a large hypodense lesion in the pons, and MRI revealed symmetric T2/T2-FLAIR hyperintensities in the central pons without mass effect or enhancement, consistent with CPM. No acute sodium shifts were identified at any point during hospitalization, supporting tacrolimus-related neurotoxicity as the primary etiology. Tacrolimus was discontinued; however, the patient subsequently developed acute liver failure secondary to allograft rejection and expired several days later.
Conclusions:
This case highlights the emerging importance of calcineurin inhibitor therapy as a cause of central pontine demyelination syndrome independent of osmotic shifts. Underlying liver dysfunction and transplant-related metabolic stress may increase susceptibility. Early recognition of neurotoxicity and careful balancing of immunosuppression are essential to optimize outcomes.
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