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Neurosciences: PsychiatryPsychiatry Posters |
1 Nuclear Medicine Section; 2 Psychiatry Clinic, University of Chile Clinical Hospital, Santiago, Chile; 3 Radiology; 4 Hematology-Oncology, Pontificia Universidad Católica de Chile, Santiago, Chile
1004
Objectives: Cocaine consumption induces cortical brain perfusion defects, but their pathophysiology is not completely understood. Vasospasm plays a role and cocaine may activate the hemostatic system. Our goal was to examine the association between hemostasis activation and brain perfusion, in patients with recent cocaine consumption and under strict abstinence.
Methods: We studied 10 cocaine dependent men (24-49 y.o.) according to DSM-IV criteria, with confirmed recent use of cocaine. Basal brain perfusion SPECT was performed and hemostasis activation assessment: P-selectin, phosphatidilserine (PS) and CD40L expression on platelets; tissue factor (TF) on circulating monocytes and circulating plasma microparticles (n°, cellular origin and procoagulant activity [PCA]) by flow cytometry, platelet PCA and thrombin antithrombin complex [TAT]).
Results: In 10/10 perfusion baseline abnormalities were significantly correlated with platelet P-selectin (r:0.69;p<0.02) and PCA in microparticles (r:0.88;p=0.007). When cut-off point was set for brain perfusion defects severity, TAT, microparticles, PS, P-Selectin and TF were significantly increased in patients with more severe parenchymal damage (75th percentile). Control SPECT performed a month later in 8/10 patients during abstinence, showed multiple small bilateral reversible foci.
Conclusions: Cocaine use activates the hemostatic system and appears to be related to severity of cortical perfusion abnormalities. Confirmation of these findings on a larger number of patients is warranted.
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