K B Nolte1, L M Brass, C F Fletterick. 1. Office of the Medical Investigator, University of New Mexico School of Medicine, Albuquerque 87131-5091, USA.
Abstract
OBJECTIVES: To determine the incidence of cocaine abuse in cases of fatal intracranial hemorrhage and to examine potential pathophysiologic mechanisms. DESIGN: Prospective clinical, autopsy, and toxicologic evaluation of all cases of fatal non-traumatic intracranial hemorrhage examined during 1 year (April 11, 1989 to April 10, 1990) at the Connecticut Office of the Chief Medical Examiner. Autopsy examination included exhaustive histologic evaluation of cerebral vessels and parenchyma for vasculitis and other vasculopathies. RESULTS: Ten of 17 (59%) of all non-traumatic intracranial hemorrhages were associated with a positive toxicology for cocaine. Seven (70%) of these were parenchymal hemorrhages, and the remaining three (30%) were subarachnoid hemorrhages (ruptured berry aneurysms). No vasculitis or other vasculopathy was identified. CONCLUSIONS: These findings implicate cocaine use as a significant risk factor for fatal brain hemorrhage and may explain, in part, the increased incidence of hemorrhagic stroke in some drug-using cohorts. The lack of specific pathologic findings suggests that cocaine-associated intracranial hemorrhages are a consequence of the pharmacodynamic effect of cocaine and not a cocaine-induced vasculopathy.
OBJECTIVES: To determine the incidence of cocaine abuse in cases of fatal intracranial hemorrhage and to examine potential pathophysiologic mechanisms. DESIGN: Prospective clinical, autopsy, and toxicologic evaluation of all cases of fatal non-traumatic intracranial hemorrhage examined during 1 year (April 11, 1989 to April 10, 1990) at the Connecticut Office of the Chief Medical Examiner. Autopsy examination included exhaustive histologic evaluation of cerebral vessels and parenchyma for vasculitis and other vasculopathies. RESULTS: Ten of 17 (59%) of all non-traumatic intracranial hemorrhages were associated with a positive toxicology for cocaine. Seven (70%) of these were parenchymal hemorrhages, and the remaining three (30%) were subarachnoid hemorrhages (ruptured berry aneurysms). No vasculitis or other vasculopathy was identified. CONCLUSIONS: These findings implicate cocaine use as a significant risk factor for fatal brain hemorrhage and may explain, in part, the increased incidence of hemorrhagic stroke in some drug-using cohorts. The lack of specific pathologic findings suggests that cocaine-associated intracranial hemorrhages are a consequence of the pharmacodynamic effect of cocaine and not a cocaine-induced vasculopathy.
Authors: Sheryl Martin-Schild; Karen C Albright; Hen Hallevi; Andrew D Barreto; Maria Philip; Vivek Misra; James C Grotta; Sean I Savitz Journal: Stroke Date: 2010-02-25 Impact factor: 7.914