Neurovascular Complications of Cocaine Use at a Tertiary Stroke Center

Department of Neurology, University of California San Francisco, CA 94143-0114, USA.
Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association (Impact Factor: 1.67). 05/2010; 19(4):273-8. DOI: 10.1016/j.jstrokecerebrovasdis.2009.05.002
Source: PubMed


An association between cocaine use and stroke has been reported, but few studies have examined cocaine-related neurovascular disease using modern stroke diagnostic techniques. We describe a large cohort of patients with cocaine-related stroke to define the pathophysiology and manifestations of cocaine-related neurovascular disease.
All adult admissions to a tertiary neurovascular service from July 1, 1998 to July 1, 2008 were screened for evidence of current or previous cocaine use. Patients included underwent thorough review of medical records including diagnostic procedure, laboratory, and imaging results.
A total of 5,142 records were screened and 96 patients were identified; 45 (47%) were given the diagnosis of ischemic stroke/transient ischemic attack (TIA), 26 (27%) with intracerebral hemorrhage (ICH), and 25 (26%) with subarachnoid hemorrhage. In all, 61 (63.5%) patients were categorized as active and 35 (36.5%) as previous cocaine users. Stroke type differed significantly between active and prior users (P=.004), with active users more likely to have ICH compared with previous users (37.7% v 8.6%) and less likely to have ischemic stroke or TIA (36.1% v 65.7%). The most common stroke/TIA cause was large artery atherosclerosis in 20 (44%) patients. Of the 25 subarachnoid hemorrhage cases, 22 (88%) were aneurysmal.
Ischemic stroke/TIA is a common neurovascular presentation in patients with a remote history of cocaine use, often as a result of atherosclerotic disease; neither vasculitis nor vasospasm was a common cause of stroke in this cohort. ICH is more common in those currently using cocaine perhaps because of acute spikes in blood pressure. Further prospective trials are needed to confirm these results.

8 Reads
  • Source
    • "Seizures are considered to be a major determinant of cocainerelated lethality in humans [4] and animals [9]. Sudden death in cocaine abuse may also be attributed to cardiac arrhythmia and intracerebral hemorrhage [10] [11]. Currently, no specific treatment modalities offer protection against cocaine-induced seizures and death in humans. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The aims of this study were to characterize the protective profile of electroacupuncture (EA) on cocaine-induced seizures and mortality in mice. Mice were treated with EA (2 Hz, 50 Hz, and 100 Hz), or they underwent needle insertion without anesthesia at the Dazhui (GV14) and Baihui (GV20) acupoints before cocaine administration. EA at 50 Hz applied to GV14 and GV20 significantly reduced the seizure severity induced by a single dose of cocaine (75 mg/kg; i.p.). Furthermore, needle insertion into GV14 and GV20 and EA at 2 Hz and 50 Hz at both acupoints significantly reduced the mortality rate induced by a single lethal dose of cocaine (125 mg/kg; i.p.). In the sham control group, EA at 50 Hz applied to bilateral Tianzong (SI11) acupoints had no protective effects against cocaine. In addition, EA at 50 Hz applied to GV14 and GV20 failed to reduce the incidence of seizures and mortality induced by the local anesthetic procaine. In an immunohistochemistry study, EA (50 Hz) pretreatment at GV14 and GV20 decreased cocaine (75 mg/kg; i.p.)-induced c-Fos expression in the paraventricular thalamus. While the dopamine D 3 receptor antagonist, SB-277011-A (30 mg/kg; s.c), did not by itself affect cocaine-induced seizure severity, it prevented the effects of EA on cocaine-induced seizures. These results suggest that EA alleviates cocaine-induced seizures and mortality and that the dopamine D 3 receptor is involved, at least in part, in the anticonvulsant effects of EA in mice.
    Evidence-based Complementary and Alternative Medicine 04/2013; 2013(1):134610. DOI:10.1155/2013/134610 · 1.88 Impact Factor
  • Source
    • "Cocaine use leads to multiple neurovascular complications [1]. Although stroke has been a well-recognized complication of cocaine use, there have been relatively few studies evaluating the radiological and clinical characteristics of spontaneous intracerebral hemorrhages (ICH) among cocaine users [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: To date there is only one single-center study that has exclusively reported characteristics, location, and outcomes of spontaneous intracerebral hemorrhages (ICH) among cocaine users. We aimed to describe the radiological location and characteristics along with clinical outcomes of spontaneous ICH in a similar population. We conducted a retrospective chart review of consecutive patients admitted to a tertiary care hospital, with a spontaneous ICH, who had a urine drug screen performed within 48 hours of admission. Exposure to cocaine was defined by a positive urine drug screen within 48 hours of hospital admission. Demographics, radiographic features of ICH, and short-term clinical outcomes of patients with a positive urine drug screen were analyzed and compared with the cocaine negative group. Among the 102 patients analyzed, 20 (19.6%) had documented exposure to cocaine. There was a predominance of males in both groups with significantly more Blacks in the cocaine positive group (P = 0.0246). A statistically significant number of patients with cocaine use had ICH in a subcortical location (P = 0.0224) when compared to cocaine negative patients. There was no difference in GCS, ICH volume, intraventricular extension, ICU days, hospital days, hospital cost, mortality, and ICH score. ICH in cocaine use is more frequently seen in the subcortical location.
    03/2013; 2013:124390. DOI:10.1155/2013/124390
  • [Show abstract] [Hide abstract]
    ABSTRACT: Drug abuse represents a significant health issue. The major substances abused include cannabis, opiates, cocaine, amphetamine, methamphetamine and 'ecstasy'. Alterations of intracellular messenger pathways, transcription factors and immediate early genes within the brain reward system seem to be fundamentally important for the development of addiction and chronic drug abuse. Genetic risk factors and changes in gene expression associated with drug abuse are still poorly understood. Besides cardiovascular complications, psychiatric and neurologic symptoms are the most common manifestations of drug toxicity. A broad spectrum of changes affecting the central nervous system is seen in drug abusers. The major findings result from the consequences of ischaemia and cerebrovascular diseases. Except for a few observations of vasculitis, the aetiology of these cerebrovascular accidents is not fully understood. The abuse of amphetamine, methamphetamine and MDMA has been related to neurotoxicity in human long-term abusers and to the risk of developing Parkinson's disease. However, whether such neurotoxicity occurs remain to be established. Systematic histological, immunohistochemical and morphometric investigations have shown profound morphological alterations in the brains of polydrug abusers. The major findings comprise neuronal loss, neurodegenerative alterations, a reduction of glial fibrillary acidic protein-immunopositive astrocytes, widespread axonal damage with concomitant microglial activation as well as reactive and degenerative changes of the cerebral microvasculature. These observations demonstrate that drugs of abuse initiate a cascade of interacting toxic, vascular and hypoxic factors, which finally result in widespread disturbances within the complex network of central nervous system cell-to-cell interactions.
    Neuropathology and Applied Neurobiology 10/2010; 37(2):118-34. DOI:10.1111/j.1365-2990.2010.01131.x · 3.93 Impact Factor
Show more