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Cocaine-induced leukoencephalopathy is a rare but serious condition. It is frequently associated with the adulterant levamisole. Levamisole toxicity can present with a variety of symptoms including neurological complications, respiratory distress, and dermatitis. Current data shows predisposition of HLA-B27-positive individuals. Here, we present a case of delayed progressive leukoencephalopathy three weeks after cocaine exposure with possible levamisole contamination.

A 54-year-old man with a history of cocaine use and psoriasis presented with a two-day course of rapidly progressive confusion, catatonia, and altered language. Approximately three weeks prior, he was hospitalized for acute hypoxic respiratory failure where extended toxicological testing revealed presence of cocaine. He was discharged without neurological deficits and refrained from further cocaine use. Detailed workup for stroke, seizures, and infectious, toxic, and metabolic causes was unrevealing. Empiric antimicrobial therapy was started until all CSF studies resulted normal with the exception of elevated protein (85 mg/dL). MRI brain revealed non-enhancing bifrontal FLAIR hyperintensities with poor grey-white-matter distinction, concerning for encephalitis, and high-dose steroids were initiated. A diffuse maculopapular rash separate from his severe psoriasis was biopsied and dermatopathology was consistent with erythema gyratum repens or erythema annulare centrifugum which can be associated with malignancy or nonspecific inflammatory/infectious conditions. Subsequent rheumatological, oncological, and paraneoplastic workup remained unrevealing. HLA-B27 was negative. Over the course of two weeks, serial MRIs showed progressive diffusion-restricting supratentorial leukoencephalopathy with increasing edema and mass effect which correlated with worsening of the patient’s neurological status to the point of akinetic mutism.