Sodium valproate - Induced skeletal myopathy

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.