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Sodium valproate -- induced skeletal myopathy

L Kasturi1, Sangeeta P Sawant

  • 1Department of Pediatrics, Bhabha Atomic Research Centre Hospital, Anushaktinagar, Mumbai, India.

Indian Journal of Pediatrics
|April 7, 2005
PubMed

Insights

Long-term sodium valproate therapy can cause carnitine deficiency, leading to skeletal myopathy in children. Supplementation with L-carnitine reversed these effects, improving muscle weakness.

Area of Science:

  • Neurology
  • Clinical Pharmacology
  • Biochemistry

Background:

  • Sodium valproate is a widely used antiepileptic drug.
  • Neurocysticercosis is a parasitic infection of the brain causing epilepsy.
  • Long-term use of sodium valproate has been associated with various side effects.

Observation:

  • A four-year-old boy with epilepsy secondary to neurocysticercosis developed limb girdle weakness.
  • Electromyography (EMG) confirmed a myopathic process.
  • Low plasma carnitine levels were detected, suggesting drug-induced carnitine deficiency.

Findings:

  • Sodium valproate therapy was identified as the likely cause of carnitine deficiency.
  • Discontinuation of sodium valproate and initiation of L-carnitine supplementation led to significant clinical improvement.
  • Plasma carnitine levels normalized after L-carnitine supplementation.

Implications:

  • This case highlights a potential adverse effect of long-term sodium valproate treatment.
  • Monitoring carnitine levels may be warranted in patients on long-term sodium valproate.
  • L-carnitine supplementation can be an effective treatment for drug-induced carnitine deficiency and myopathy.

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