Central Pontine Myelinolysis in a Child: Clinical Case

Background. Central pontine myelinolysis (CPM) is limited symmetric non-inflammatory demyelination in the middle part of pontine. This disease is based on electrolyte balance disorders. Although CPM was firstly described in adults, but it can also occur in children. Every new case of CPM in children has undeniable interest and high scientific and practical significance due to its low incidence. Clinical case description. The child, 7 years old, had acute development, lethargy, multiple vomiting, subfebrile fever, pains in epigastric region. It has happened after drinking an unknown herb growing in the yard and previously covered with the insecticide "Akarin", according to the mother. The child was hospitalized in the pediatric department at the place of residence. The patient developed strabismus, swallowing disorder, and muscle weakness on infusion therapy. Biochemical blood test has shown hypokalemia and hyponatremia. Head MRI has shown symmetrical focal lesion of heterogeneous structure in pontine. Conclusion. Distinctive feature of this case is the development of CPM in a child on the ongoing therapy of hypokalemia and hyponatremia. The timely provision of qualified medical care has favoured the child's recovery.

Topiramate-induced severe electrolyte abnormalities and hypernatremia leading to central pontine myelinolysis

Central pontine myelinolysis (CPM) develops due to acute hypernatremia from a normal baseline serum sodium in the setting of electrolyte abnormalities induced by topiramate use. Topiramate is a commonly used medication with several indications including migraines, myoclonic jerks and seizures. It has been reported to cause renal tubular acidosis and severe electrolyte abnormalities, which in turn predispose patients to neuropathology via renal concentration defects and osmotic shifts. Our patient is a 55-year-old woman with a history of multiple sclerosis and myoclonus on topiramate for several years who presented with weakness and was found to be profoundly hypokalemic. She went on to develop changes in mental status, motor deficits and evidence of CPM on MRI during her hospitalisation. Surprisingly, the patient never had hyponatremia; however, she had an acute rise in serum sodium from a normal baseline after fluid resuscitation with normal saline for hypotension during her admission.