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Selenium deficiency triggering intractable seizures

V T Ramaekers1, M Calomme, D Vanden Berghe

  • 1Department of Paediatric Neurology, University of Aachen, Germany.

Neuropediatrics
|August 1, 1994
PubMed
Summary
This summary is machine-generated.

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Severe neurodevelopmental issues and intractable seizures in children were linked to selenium deficiency. Selenium supplementation improved seizures and liver function, suggesting its crucial role in neuronal health.

Area of Science:

  • Biochemistry
  • Neurology
  • Pediatrics

Background:

  • Investigating severe neurodevelopmental retardation and intractable seizures in infants.
  • Ruling out common neurometabolic disorders as the cause.

Observation:

  • Two children presented with intractable seizures and elevated liver function tests within the first year of life.
  • Systemic selenium deficiency was documented concurrently with seizure onset.
  • One infant died at ten months with neuropathology consistent with Progressive Neuronal Degeneration of Childhood (PNDC) / Alpers disease.

Findings:

  • Selenium deficiency was implicated in intractable seizures and neuronal damage.
  • Oral selenium supplementation (3-5 µg/kg) led to seizure reduction and EEG improvement.
  • Liver function normalized following selenium supplementation in both patients.

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Implications:

  • Selenium deficiency may trigger intractable seizures and subsequent neuronal damage in susceptible individuals.
  • Seleno-dependent enzymes like Glutathione Peroxidase (GPX) and Phospholipid Hydroperoxide Glutathione Peroxidase (PHGPX) are vital for neuronal defense against oxidative stress.
  • This study highlights the critical role of selenium in pediatric neurological health and warrants further investigation into selenium's impact on epilepsy and neurodegenerative disorders.