Delayed-Onset Movement Disorder and Encephalopathy After Oxycodone Ingestion

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We present the case of a 14-year-old girl with a biphasic course after oxycodone ingestion. Clinically, she had a rapid return to baseline after initial ingestion and presented a week later with new-onset ballism, akathisia, and encephalopathy. Neuroimaging demonstrated bilateral globi pallidi and cerebellar lesions with a relative decrease of metabolite peaks on magnetic resonance spectroscopy. Her movement disorder was treated successfully with valproic acid and clonidine. Her cognitive functioning returned to baseline 3 months after ingestion.

Introduction

Heroin-induced leukoencephalopathy was first described in 1988 when patients developed a spongiform leukoencephalopathy following heroin inhalation.1 Affected patients experience a delayed clinical syndrome of cerebellar signs, akathisia, and apathy that can present up to 3 weeks after the last inhalation of heroin, and in some cases, it progresses to death. Neuroimaging in these patients reveals characteristic involvement of the posterior cerebral white matter, medial lemniscus of the brainstem, cerebellar white matter, and posterior limb of the internal capsule.2, 3 The etiology is suspected to be due to toxic injury; however, the causative agent (eg, the heroin or a contaminant) has yet to be identified.1, 2, 3, 4

More recently, several case reports have described an acute toxic encephalopathy related to methadone or oxycodone ingestion that preferentially affects the bilateral globi pallidi and cerebellar gray matter that at times can lead to acute obstructive hydrocephalus.5, 6, 7, 8 The imaging pattern distinguishes them from typical hypoxic injury; however, there is an overlap between the two etiologies, which can both also result in a delayed leukoencephalopathy, making a distinction between the two etiologies challenging at times. One case of methadone toxicity with a biphasic clinical presentation of encephalopathy and imaging consistent with toxic injury has been described.9 To our knowledge, there have been no documented cases of oxycodone ingestion with a biphasic clinical encephalopathy and a radiographic picture consistent with an acute toxic injury. We present a case of an adolescent girl with acute neuroimaging changes with a biphasic clinical course following oxycodone ingestion.

Section snippets

Case Report

A 14-year-old Indian American girl presented to the emergency department with altered mental status and decreased respiratory effort. She was last seen with an intact neurological status at 11:30 pm the evening before presentation. At 9:30 am the next morning, she was found by her parents unresponsive with agonal respirations. She had ingested 15 5-mg tablets of oxycodone. Her father began chest compressions as he was unable to find a pulse, and emergency medical services arrived 4 minutes later

Discussion

The patient presented with neurological findings that localized to the basal ganglia. Our differential diagnosis included postanoxic chorea, a toxic-metabolic syndrome, autoimmune movement disorder, hyperthyroidism, and conversion disorder. Findings of laboratory and imaging evaluation narrowed our differential diagnosis to postanoxic injury or a toxic encephalopathy.

The specific imaging findings of T2 and FLAIR hyperintensity with corresponding T1 hyperintensity of the bilateral globi pallidi,

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