Heroin-induced leukoencephalopathy

Case contributed by Francis Deng
Diagnosis certain

Presentation

Polysubstance user including 12-year history of inhaled heroin, now presenting with dysarthria, ataxia, left-sided weakness, spasticity, and cognitive changes.

Patient Data

Age: 30 years
Gender: Male

Extensive symmetric T2 prolongation in the white matter including perirolandic subcortical white matter, central and posterior parts of the centrum semiovale and corona radiata, occipital white matter, splenium and posterior body of the corpus callosum, occipital lobe white matter, cerebral peduncles, tracts in the brainstem, and cerebellar white matter.

5 months after presentation

ct

Extensive, marked hypoattenuation of bilateral symmetric cerebral and cerebellar white matter corresponding to findings on prior MRI.

Case Discussion

The history of long-term heroin abuse, urine toxicology positive for 6-acetylmorphine, and imaging findings of a posterior predominant, confluent, symmetric white matter abnormality were suggestive of spongiform toxic leukoencephalopathy due to long-term heroin vapor inhalation, a method known as "chasing the dragon." Because of polysubstance abuse (including cocaine and alcohol) and polyroute use of heroin (smoking and chasing the dragon per chart history), this case met only the proposed strict definition for "possible" chasing the dragon leukoencephalopathy 1. However, these other drugs of abuse are frequent bystanders that rarely cause leukoencephalopathy, and chasing the dragon is often conflated with smoking inadvertently, so the presumptive clinical diagnosis remained chasing the dragon leukoencephalopathy.

A lumbar puncture and HIV testing were normal. He was treated with antioxidant supplementation including coenzyme Q, vitamin C, and vitamin E.

Over the next half-year, the patient continued to decline neurologically despite abstinence from drug use, a phenomenon known as "coasting." He developed spastic quadriparesis, autonomic dysfunction such as central pyrexia, and akinetic mutism. He was discharged on hospice but then began to make a neurologic recovery. With intensive physical, occupational, and speech therapy, at five-year follow-up, he had regained his ability to speak and walk. He still had mild to moderate dysarthria, limb contractures, and dependence on assistance for instrumental activities of daily living.

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