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Published on: February 18, 2016
Use of levamisole-adulterated cocaine is associated with increased load of white matter lesions
Florian Conrad1, Sarah Hirsiger1, Sebastian Winklhofer1
1From the Department of Neurology, University Hospital Zurich, University of Zurich, Switzerland (Conrad, Wegener); the Department of Psychiatry, Psychotherapy, and Psychosomatics, Psychiatric University Hospital, University of Zurich, Switzerland (Hirsiger, Stämpfli, Seifritz, Quednow); the Department of Neuroradiology, University Hospital Zürich, University of Zurich, Switzerland (Winklhofer); the Center of Forensic Hair Analytics, Institute of Forensic Medicine, University of Zurich, Switzerland (Baumgartner); and the Neuroscience Center Zurich, University of Zurich and Swiss Federal Institute of Technology Zurich, Switzerland (Seifritz, Wegener, Quednow).
Background:
Cocaine use has been associated with vascular pathologies, including cerebral white matter hyperintensities. Street cocaine is most often adulterated with levamisole, an anthelminthic drug that may also be associated with vascular toxicity. However, whether levamisole exposure from cocaine consumption further accelerates the development of white matter lesions remains unknown.
Methods:
We investigated the association of cocaine and levamisole exposure with white matter hyperintensities in 35 chronic cocaine users and 34 healthy controls. We measured cocaine and levamisole concentrations in hair samples, which reflected exposure up to 6 months previously. We assessed the number and total surface area of the white matter hyperintensities using structural MRI (FLAIR sequence). Using generalized linear models, we analyzed the contributions of cocaine and levamisole to the number and area of white matter hyperintensities, accounting for several confounding factors.
Results:
Analysis using generalized linear models revealed that cocaine users had more white matter hyperintensities in terms of total surface area, but not in terms of number. Further generalized linear models that included cocaine and levamisole hair concentrations (instead of group) as predictors indicated that levamisole exposure was strongly associated with more and larger white matter hyperintensities, suggesting that the elevated white matter hyperintensities in cocaine users were driven mainly by levamisole exposure. Finally, white matter hyperintensities in levamisole-exposed cocaine users were located primarily in the periventricular and juxtacortical white matter.
Limitations:
The sample size was moderate, and blood pressure was not systematically assessed.
Conclusion:
As an adulterant of cocaine, levamisole appears to increase the risk of white matter injury.
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