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Delayed-onset movement disorder and encephalopathy after oxycodone ingestion
Christopher W Beatty1, Ping-Ru Ko1, Jason Nixon2
1Department of Neurology, University of Washington, Seattle, WA; Division of Neurology, Seattle Children's Hospital, Seattle, WA.
Seminars in Pediatric Neurology
|August 24, 2014
Summary
A 14-year-old experienced a delayed neurological reaction to oxycodone, developing movement disorders and encephalopathy a week after ingestion. Treatment with valproic acid and clonidine successfully resolved her symptoms.
Area of Science:
- Neurology
- Toxicology
Background:
- Oxycodone, an opioid analgesic, can cause various adverse effects.
- Delayed neurological sequelae following overdose are rare but significant.
Observation:
- A 14-year-old female presented with a biphasic clinical course after oxycodone ingestion.
- Initial recovery was followed by delayed onset of ballism, akathisia, and encephalopathy.
- Neuroimaging revealed characteristic lesions in the globus pallidus and cerebellum.
Findings:
- Magnetic resonance spectroscopy showed decreased metabolite peaks in affected brain regions.
- The movement disorder and encephalopathy were successfully treated with valproic acid and clonidine.
- Full cognitive recovery was observed at 3 months post-ingestion.
Implications:
- This case highlights the potential for delayed neurotoxicity from oxycodone.
- Valproic acid and clonidine may be effective treatments for oxycodone-induced movement disorders.
- Understanding biphasic neurotoxic effects is crucial for managing overdose cases.
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