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Sodium valproate - Induced skeletal myopathy.
L Kasturi1, Sangeeta P Sawant2
1Department of Pediatrics, Bhabha Atomic Research Centre Hospital, Anushaktinagar, 400 094, Mumbai, Maharashtra, India.
Indian Journal of Pediatrics
|April 6, 2017
Summary
Long-term sodium valproate therapy can cause carnitine deficiency myopathy in children. Supplementation with L-carnitine led to significant recovery in a young boy with epilepsy.
Area of Science:
- Neurology
- Clinical Case Study
- Pharmacology
Background:
- Sodium valproate is a widely used antiepileptic drug.
- Neurocysticercosis can lead to secondary epilepsy.
- Long-term use of sodium valproate has been associated with metabolic disturbances.
Purpose of the Study:
- To report a case of skeletal myopathy in a child treated with sodium valproate.
- To investigate the potential link between sodium valproate and carnitine deficiency.
- To evaluate the efficacy of L-carnitine supplementation in treating this condition.
Main Methods:
- Clinical presentation and neurological examination of a four-year-old boy.
- Electromyography (EMG) to assess muscle function.
- Measurement of plasma carnitine levels.
- Monitoring of clinical response after sodium valproate withdrawal and L-carnitine supplementation.
Main Results:
- The patient presented with limb girdle weakness and EMG-confirmed myopathy.
- Low plasma carnitine levels were detected, suggesting drug-induced deficiency.
- Discontinuation of sodium valproate and initiation of L-carnitine supplementation resulted in marked clinical improvement.
- Plasma carnitine levels normalized following supplementation.
Conclusions:
- Sodium valproate therapy can induce carnitine deficiency myopathy.
- Carnitine deficiency should be considered in patients on long-term valproate therapy presenting with myopathic symptoms.
- L-carnitine supplementation is an effective treatment for reversing valproate-induced carnitine deficiency myopathy.