Original Article
Cerebrovascular Complications of the Use of the Crack Form of Alkaloidal Cocaine
N Engl J Med 1990; 323:699-704September 13, 1990
- Abstract
- Abstract
Background and Methods.
The use of cocaine, especially one of its alkaloidal forms ("crack"), has been increasingly associated with cerebrovascular disease. To clarify the clinical, radiologic, and pathological features of the events associated with cocaine use, we identified 28 patients at four medical centers who had stroke temporally related to the use of alkaloidal cocaine (during or within 72 hours of use).
Results.
The 28 patients had the following types of cerebrovascular event: cerebral infarction (n = 18[2hemorrhagic; 1 fatal]) in the areas supplied by the middle cerebral artery (n = 10), anterior cerebral artery (n = 3), posterior cerebral artery (n = 1 ), and vertebrobasilar arteries (n = 4); subarachnoid hemorrhage (n = 5); intraparenchymal hemorrhage (n = 4); and primary intraventricular hemorrhage (n = 1). Eighteen patients (64 percent) had acute neurologic symptoms immediately or within one hour of using cocaine. Fifteen patients (45 percent) with either occlusive or hemorrhagic strokes had severe headache as an early symptom. Vasculitis was not suggested by radiography in any patient, nor was it identified on pathological examination in one patient who died. All the patients were young (mean age, 34 years; range, 23 to 49) and had no other apparent, direct cause of stroke. Other risk factors for stroke among the patients included mild mitral-valve prolapse (n = 4), hypertension (n = 4), cigarette smoking (n = 8), and regular alcohol use (n = 6).
Conclusions.
There is a strong temporal association of the use of alkaloidal cocaine with both ischemic and hemorrhagic cerebrovascular events. Cocaine-related stroke probably has many causes. A thorough history focusing on the use of cocaine and toxicologic screening of urine and serum should be part of the evaluation of any young patient with a stroke. (N Engl J Med 1990; 323:699–704.)
Media in This Article
Table 1
Cerebrovascular Complications of the Use of Alkaloidal Cocaine (Crack).*Table 2
Types of Cerebrovascular Events in 28 Patients.Article Activity
- Article
NUMEROUS studies have demonstrated an association between cerebrovascular disease and the use of cocaine.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 The appearance in 1983 of commercially prepared alkaloidal cocaine ("crack") escalated an already existing cocaine epidemic.1 , 10 , 35 36 37 Reports of medical complications of cocaine use, including stroke, have increased as well, although it is unclear whether recent reports of stroke among crack users reflect the spreading epidemic, greater cerebrovascular specificity, higher potency, or a combination of these factors. "Freebasing" (preparing the extract of the almost pure alkaloidal, or freebase, form of the drug) removes cocaine adulterants.38 By contrast, crack is made simply by heating an aqueous solution of cocaine hydrochloride with sodium bicarbonate or ammonia; the resulting precipitate, unlike freebase cocaine, contains adulterants but is also smokable.
Despite the current widespread use of cocaine, little is known about the detailed clinical, radiologic, and pathological features of the cerebrovascular syndromes associated with use of the alkaloidal form of cocaine. We therefore studied 28 patients with a variety of cerebrovascular complications of the use of crack.
Methods
Patients known to have cerebrovascular complications temporally related to the use of alkaloidal cocaine (i.e., occurring during or within 72 hours of use) were identified at four clinical centers. Those seen at Henry Ford Hospital were studied prospectively, as were those seen at the University of Miami; patients seen at Harlem Hospital Center and the New York Neurological Institute were studied either prospectively or retrospectively (for this report, the patients seen at this center have been combined); and those seen at Yale Medical School were studied retrospectively. Patients were considered to have smoked crack cocaine if they or someone accompanying them gave a confirmatory history, supported by the results of toxicologic testing when it was performed. Toxicologic testing of urine was performed with the enzyme-multiplication immunoassay technique or thin-layer chromatography, and confirmatory toxicologic testing of serum was performed with gas chromatography-mass spectrometry. Alternatively, when toxicologic studies of urine or serum showed cocaine or a cocaine metabolite, the patients were asked about cocaine use. Patients were excluded from the study if they had used cocaine hydrochloride (the nonalkaloidal form of cocaine) in the recent past or if the nature of their cocaine use was in doubt. All patients were seen during a 47-month period from January 1986 through November 1989. Their medical histories included information on the duration and extent of use of other substances and other risk factors for stroke. All the patients were examined by a neurologist, who directed the subsequent evaluation.
A diagnosis of cerebral infarction was made when an acute focal neurologic deficit persisted longer than 24 hours and neither computed tomography (CT) of the head nor examination of the cerebrospinal fluid revealed the presence of blood, or when the history, physical examination, and radiologic studies were highly suggestive of stroke (e.g., the patient did not have headache and infarction was seen on CT of the head) in the absence of cerebrospinal fluid analysis. A cerebral infarction was classified as unconfirmed when the patient had an acute focal neurologic syndrome within a vascular territory with relatively rapid clinical improvement in the absence of meningeal signs and when cerebrospinal fluid analysis was not performed. Intracerebral hemorrhage was diagnosed on the basis of CT or magnetic resonance imaging of the head.
Results
Twenty-eight patients had cerebrovascular events temporally related to the use of alkaloidal cocaine (Tables 1Table 1
Cerebrovascular Complications of the Use of Alkaloidal Cocaine (Crack).** and 2Table 2Types of Cerebrovascular Events in 28 Patients.); three of these patients were included in a previous report.9 The patients' mean age was 34 years (range, 23 to 49). Eighteen patients (64 percent) were men. Twenty-four patients (86 percent) were black. Six patients (21 percent) had a blood pressure greater than 150/100 mm Hg at the time of the initial evaluation. Eighteen (64 percent) had acute neurologic symptoms immediately or within one hour of using crack. Symptoms developed between one and three hours after use in five patients (18 percent). Stroke occurred two to three days after the use of crack in two, and the timing of the last cocaine use was uncertain, but known to be within two to three days, in the cases of the remaining three patients. Fifteen patients (54 percent), who had either occlusive or hemorrhagic strokes, had severe headache as an early symptom. Five (18 percent) had seizures either before or in conjunction with their strokes (two who had cerebral infarction and one each with hemorrhagic infarction, intraventricular hemorrhage, and intracerebral hemorrhage with rupture into the lateral ventricle). Inmost cases the seizures heralded the onset of stroke, and in one patient the seizure followed headache and left hemiparesis.Four patients (14 percent) had a history of hypertension (but several patients had had no previous medical evaluation), and one patient each had a history of treated syphilis, sickle cell disease, Stage I pulmonary sarcoidosis, migraine, hyperglycemia, and two previous myocardial infarctions associated with the use of crack six years earlier. Two women were pregnant (at two months' and eight months' gestation) at the time of their strokes.
The most common cerebrovascular complication of the use of alkaloidal cocaine was cerebral infarction, documented in 18 patients (64 percent) (Table 2). The territories of the middle cerebral artery (n = 10), anterior cerebral artery (n = 3), posterior cerebral artery (n = 1), and vertebrobasilar arteries (n = 4) were affected. Involvement of the middle cerebral artery was equally divided between the territories of deep perforating lenticulostriate vessels and superficial—pial vessels. Two of the patients with cerebral infarction had hemorrhagic transformation of their infarcts two to three days after the initial CT scan; neither was receiving anticoagulation therapy. Three patients (11 percent) had transient ischemic attacks (multiple and Stereotypic in all) in association with crack use before their ischemic strokes. Ten patients (36 percent) had intracranial hemorrhage: in five (18 percent) it was subarachnoid, in four (15 percent) intracerebral, and in one (4 percent) intraventricular.
The duration of continuous crack smoking ranged from 1 to 36 hours; up to 16 g was smoked within a few hours of the stroke. Most patients had been regular crack users for at least two years before their strokes, although one had smoked crack only occasionally, and one had used it for the first time.
Two patients had used intravenous heroin 8 and 20 years earlier, and one patient had used heroin 10 days before the stroke. One patient had used cocaine hydrochloride 10 years earlier. Alcohol was ingested within a day of the stroke by five patients, although it was detected in the blood of only one. Ten patients (36 percent) had a history of recent tobacco use, and two others had nicotine in their urine. Two patients had quinine in their urine. Codeine was present in the urine of two patients, who had taken it for headache. One patient had smoked marijuana with crack. For 11 patients (39 percent), only cocaine or its metabolite was identified on toxicologic screening. Toxicologic screening was performed for a total of 16 patients (57 percent).
All 28 patients underwent CT investigation of the head. Six patients also had magnetic resonance imaging of the head. Sixteen of the CT scans (57 percent) were abnormal; the location of the lesion was consistent with the results of the neurologic examination in all 16 cases. One patient had hemorrhagic changes within a right parietal infarct, detected on magnetic resonance imaging but not CT scanning, and another had subcortical white-matter infarcts seen only on magnetic resonance imaging. Several deep subcortical and brain-stem infarcts had the appearance of "lacunar" strokes on CT and magnetic resonance imaging. Intracerebral hemorrhages occurred in both deep locations (occasionally rupturing into the lateral ventricle) and lobar locations.
Cerebral angiograms were performed one to six days after the stroke in 6 of the 10 patients with intracranial hemorrhage and 9 of the 18 patients with cerebral infarction. Of the 15 angiograms, 10 (67 percent) were normal. Four patients with intracranial hemorrhage had normal cerebral angiograms (three with subarachnoid hemorrhage and one with intracerebral hemorrhage), one was found to have a small, deep cerebrovascular malformation, and one had an aneurysm of the intracranial internal carotid-artery bifurcation. Three angiograms in patients with ischemic stroke demonstrated arterial or intraarterial abnormalities: a large intraluminal clot in the proximal extracranial internal carotid artery (the artery was normal on surgical thrombectomy), a narrowed proximal posterior cerebral artery with possible occlusion of the middle cerebral artery, and a narrowed, possibly recanalized, middle-cerebral-artery branch. Vasculitis was not suggested by any of the angiographic data.
Cerebrospinal fluid from 12 patients was examined. It was normal in nine patients with cortical, subcortical, or brain-stem infarcts. Two patients (Patients 10 and 24) had cerebrospinal profiles suggesting minimal subarachnoid hemorrhage. Cerebral blood flow, measured in one patient with an ischemic stroke, revealed mild biparietal oligemia.
One patient who died was examined at autopsy. The left intracranial carotid, middle cerebral, and anterior cerebral arteries were found to be smaller than their right-sided counterparts, but the vessels were histologically normal. Histopathological examination of many sections of the left common and internal carotid and middle and anterior cerebral arteries revealed normal endothelium, intima, media, elastic lamina, and adventitia. There was hemorrhagic infarction in the territories of the left anterior and middle cerebral arteries. The aortic arch and the heart were normal.
No abnormalities were consistently identified on laboratory or other testing of the 28 patients. One patient had a positive low-titer antinuclear antibody, four had mild mitral-valve prolapse on echocardiography, three had left ventricular hypertrophy (including one with mild aortic-root dilatation), one had elevated serum IgG and IgA levels, and two (one with Stage I sarcoidosis) had elevated serum levels of angiotensin-converting enzyme. There was no evidence of hypercoagulability in any of the patients on the basis of the complete blood count, platelet count, prothrombin time, or activated partial thromboplastin time (measured in most of the patients). In five patients extensive coagulation studies were performed, including most if not all of the following: coagulation-factor assays; bleeding time; measurements of fibrinogen, protein S, protein C, and antithrombin III; kaolin clotting time; modified Russell's viper venom time; measurements of anticardiolipin antibodies (IgG and IgM); platelet-function studies and Sonoclot; and measurements of fibrinopeptide A, plasminogen, platelet factor 4, and beta-thromboglobulin.
*See NAPS document no. 04796 for eight pages of supplementary material. Order from NAPS c/o Microfiche Publications, P.O. Box 3513, Grand Central Station, New York, NY 10163–3513. Remit in advance (in U.S. funds only) $7.75 for photocopies or $4 for microfiche. Outside the U.S. and Canada add postage of $4.50 ($1.50 for microfiche postage).
Discussion
Our findings in this series of patients suggest that there is a strong temporal, if not causal, association of the use of alkaloidal cocaine with both ischemic and hemorrhagic cerebrovascular events. Cocaine has been associated with infarction at all levels of the central neuraxis, including the spinal cord and the retina6 , 7 , 9 , 10 , 12 13 14 , 16 , 17 , 29 30 31 32 33 , 39 40 41 42; hemorrhagic strokes have been intraparenchymal (lobar, deep, or bilateral), intraventricular, or subarachnoid.4 , 7 , 11 12 13 14 , 16 , 18 19 20 21 22 , 25 , 26 , 28 , 43 44 45 46 In reviewing 63 cases of stroke temporally associated with either the alkaloidal (n = 17) or the hydrochloride (n = 46) form of cocaine that were reported from 1977 through July 1989, we found that ischemic and hemorrhagic strokes were reported with nearly equal frequency in association with the use of alkaloidal cocaine, whereas the use of cocaine hydrochloride was more often associated with intracranial hemorrhage (in approximately 80 percent of the cases), about half the time from ruptured cerebral saccular aneurysms or vascular malformations. Only hemorrhagic stroke has been reported in association with the intravenous use of cocaine hydrochloride. The basis for these differences is unclear.
Cerebral angiographic abnormalities identified in patients with cocaine-associated cerebral infarction include single or multiple intracranial large-vessel stenosis or occlusion, possible occlusion of the extracranial internal carotid artery, vasospasm, intraluminal clot in the internal carotid artery (possibly related to vasoconstriction in large extracranial vessels and subsequent stasis), "beading," and, in approximately half the patients, normal vessels.6 , 7 , 9 , 10 , 12 13 14 , 30 , 31 , 41
In contrast to amphetamines, which cause an inflammatory vasculopathy with vessel-wall necrosis potentially leading to vessel-wall rupture and hemorrhage,47 , 48 cocaine rarely31 if ever causes frank vasculitis. This difference may explain the higher incidence of cerebrovascular anomalies and saccular aneurysms in association with cocaine-related intracranial hemorrhage.49
Cocaine is approximately 90 percent metabolized by means of rapid hydrolysis by plasma and liver cholinesterases and has a plasma half-life of about one hour.50 , 51 Cocaine metabolite may be extracted from the urine of a novice adult user for up to 48 hours after a single intranasal use52 , 53 and for up to three weeks after long-term heavy use.54 The pharmacokinetics of cocaine and its metabolites varies widely both within and among subjects.50
The cardiovascular effects of cocaine include acute hypertension, which could lead to hemorrhagic stroke, and cardiac arrhythmias53 , 55 and cardiomyopathy,56 57 58 which could produce brain infarction resulting from cardiac embolism. Loss of consciousness is common shortly after snorting or smoking large amounts of cocaine.59 Another possible mechanism for cocaine-related stroke is direct cerebral vasoconstriction.50 , 51 Cocaine prevents norepinephrine reuptake60 and may reduce the regional cerebral blood flow,61 possibly by increasing cerebrovascular resistance.62 , 63 Cocaine-associated subcortical infarcts cannot be distinguished by CT from those associated with hypertensive small-vessel disease. Cocaine-induced hypertension is transient, however, and thus acute vasoconstriction of the vessels around the circle of Willis may be the basis for these infarcts. Cocaine-induced coronary-artery vasoconstriction has been demonstrated in humans, and animal studies suggest that cocaine affects vascular smooth muscle, both indirectly, through the blockade of norepinephrine reuptake at sympathetic-nerve terminals, and directly, through its action on calcium flux.64 , 65 Cocaine also enhances the response of platelets to arachidonic acid, possibly leading to increased thromboxane production and platelet aggregation.66 Cocaine-induced vasoconstriction followed by reperfusion of initially ischemic brain is another potential mechanism of hemorrhagic stroke.67 Cerebral arterial vasoconstriction by cocaine and its metabolites has been demonstrated.68 Cocaine-induced arteriopathy has been produced experimentally.69 , 70
Our study did not directly address the issue of which persons may be predisposed to or more likely to have cerebrovascular disease after using alkaloidal cocaine. The frequent occurrence of cerebrovascular anomalies in patients who have intracranial hemorrhage after cocaine use suggests that patients with cerebral aneurysms or vascular malformations may be more likely to have intracranial hemorrhage after using cocaine. Further study will be needed to determine whether other factors, such as hypertension, cigarette smoking, alcohol use, or genetic influence, predispose persons to cocaine-associated stroke or predict or correlate with such events.
We believe that the ongoing crack epidemic will lead to more cocaine-related strokes. A thorough history of drug use and toxicologic testing of urine and serum should be part of the evaluation of any young patient with a stroke.
Supported in part by a grant (NS23393) from the National Institutes of Health and by a grant from the American Heart Association, Michigan Affiliate.
We are indebted to Hally Summers for assistance in the preparation of the manuscript and to Dr. Nabih M. Ramadan for help in translation (ref. 28).
Source Information
From the Center for Stroke Research, Department of Neurology (S.R.L., N.F., C.H.M., J.F.S., K.M.A.W.), and the Department of Pathology, Division of Neuropathology (K.-L.H.), Henry Ford Hospital and Health Science Center, Detroit; the Department of Neurology, College of Physicians and Surgeons, Columbia University, Harlem Hospital Center and Neurological Institute, New York (J.C.M.B., D.B.); the Department of Neurology, University of Miami School of Medicine, Miami (N.F., C.H.M.); the Yale Stroke Program, Department of Neurology, Yale University School of Medicine, New Haven, Conn. (L.M.B., P.F.); and the Division of Biostatistics and Research Epidemiology, Henry Ford Hospital, Southfield, Mich. (L.R.S.). Address reprint requests to Dr. Levine at the Center for Stroke Research, Department of Neurology, K-11, Henry Ford Hospital and Health Science Center, 2799 W. Grand Blvd., Detroit, MI 48202–2689.
- References
References
1
Cregler
Full Text | Web of Science | Medline2
Brust
Medline3
Caplan
CrossRef | Web of Science | Medline4
Lichtenfeld
Web of Science | Medline5
Schwartz
Web of Science | Medline6
Golbe
Web of Science | Medline7
Lowenstein
CrossRef | Web of Science | Medline8
Wojak
CrossRef | Web of Science | Medline9
Levine
Web of Science | Medline10
Levine
CrossRef | Web of Science | Medline11
Mangiardi
CrossRef | Web of Science | Medline12
Mody
Web of Science | Medline13
Jacobs
Web of Science | Medline14
Rowley
Web of Science | Medline15
Kaku
Web of Science | Medline16
Klonoff
Web of Science | Medline17
Meza
Medline18
Nalls
CrossRef | Web of Science | Medline19
Green
CrossRef | Web of Science | Medline20
Nolte
Web of Science | Medline21
Henderson
CrossRef | Web of Science | Medline22
Mercado
Web of Science | Medline23
Lundberg
Medline24
Mittleman
Web of Science | Medline25
Cregler
Medline26
Altés-Capellà
Medline27
Lehman 28
De Broucker
Web of Science | Medline29
De Vore
Web of Science | Medline30
Kaye
CrossRef | Web of Science | Medline31
Krendel
Web of Science | Medline32
Engstrand 33
Moore 34
Weingarten
CrossRef | Web of Science35
"Crack ." Med Lett Drugs Ther 1986; 28:69–70.
Web of Science | Medline36
Washton 37
Zylke
CrossRef | Web of Science | Medline38
Shannon
CrossRef | Web of Science | Medline39
Chasnoff
CrossRef | Web of Science | Medline40
Devenyi
Web of Science41
Rowbotham
Medline42
Seaman
CrossRef | Web of Science | Medline43
Peterson 44
Tardiff
Web of Science | Medline45
Rogers
Web of Science | Medline46
Spires
CrossRef | Web of Science | Medline47
Citron
Full Text | Web of Science | Medline48
Rumbaugh
Web of Science | Medline49
Brust JCM. Stroke and drugs. In: Toole JF, ed. Vascular diseases, Part III. Vol. 55 of Handbook of clinical neurology. Rev. series 11. Amsterdam: Elsevier Science, 1989:517–31.
50
Grabowski J, ed. Cocaine: pharmacology, effects and treatment of abuse. NIDA research monograph series 50. Washington, D.C.: Government Printing Office, 1984. (DHS publication no. (ADM) 84–1326.)
51
Mule SJ, ed. Cocaine: chemical, biological, clinical, social and treatment aspects. CRC drug dependence series. Cleveland: CRC Press, 1976.
52
Barnett
CrossRef | Web of Science | Medline53
Chow
CrossRef | Web of Science | Medline54
Weiss
CrossRef | Web of Science | Medline55
Pitts
CrossRef | Web of Science | Medline56
Weiner
CrossRef | Web of Science | Medline57
Karch
Web of Science | Medline58
Chokshi
Web of Science | Medline59
Schwartz
CrossRef | Web of Science | Medline60
De La Lande
CrossRef | Web of Science | Medline61
Volkow
CrossRef | Web of Science | Medline62
MacKenzie
Web of Science | Medline63
King
CrossRef | Web of Science | Medline64
Lange
Full Text | Web of Science | Medline65
Isner
Full Text | Web of Science | Medline66
Togna
Medline67
Caplan
Web of Science | Medline68
Powers 69
Langner RO, Bement CL, Perry LE. Arteriosclerotic toxicity of cocaine. In: Clouet D, Asghar K, Brown R, eds. Mechanisms of cocaine abuse and toxicity. NIDA research monograph series 88. Washington, D.C.: Government Printing Office, 1987:325–36. (DHS publication no. (ADM) 88–1585.)
70
Bement
- Citing Articles (80)
Citing Articles
1
SARA SANTOS, M. TERESA BRUGAL, GREGORIO BARRIO, YOLANDA CASTELLANO, ANTONIA DOMINGO-SALVANY, ALBERT ESPELT, M. JOSE BRAVO, LUIS DE LA FUENTE, . (2012) Assessing the effect of patterns of cocaine and alcohol use on the risk of adverse acute cocaine intoxication. Drug and Alcohol Reviewno-no
CrossRef2
M. Barbieux, O. Véran, O. Detante. (2012) Accidents vasculaires cérébraux ischémiques du sujet jeune et toxiques. La Revue de Médecine Interne 33:1, 35-40
CrossRef3
Young Hoon Sung, Perry F. Renshaw. 2011. Anatomical and Neurochemical Evidence of Neurotoxic Changes in Psychostimulant Abuse and Dependence. , 235-259.
CrossRef4
Scott M. Friedman, Curtis E. Margo, Mark Konicki, Michael Campanelli, Lee M. Jampol, Oren Z. Plous. (2011) BILATERAL VASCULAR OCCLUSIONS OF THE ANTERIOR VISUAL PATHWAY AND COCAINE ABUSE. Retinal Cases & Brief Reports 4:2, 95-98
CrossRef5
Pratik Bhattacharya, Sharief Taraman, Lakshmi Shankar, Seemant Chaturvedi, Ramesh Madhavan. (2011) Clinical Profiles, Complications, and Disability in Cocaine-Related Ischemic Stroke. Journal of Stroke and Cerebrovascular Diseases 20:5, 443-449
CrossRef6
Larry B. Goldstein, Ralph L. Sacco. 2011. Primary Prevention of Stroke. , 242-251.
CrossRef7
John C.M. Brust. 2011. Stroke and Substance Abuse. , 790-813.
CrossRef8
Carlos S. Kase, Steven M. Greenberg, J.P. Mohr, Louis R. Caplan. 2011. Intracerebral Hemorrhage. , 531-588.
CrossRef9
N. Venkatanarasimha, B. Rock, R.D. Riordan, C.A. Roobottom, W.M. Adams. (2010) Imaging of illicit drug use. Clinical Radiology 65:12, 1021-1030
CrossRef10
Shahed Toossi, Christopher P. Hess, Nancy K. Hills, S. Andrew Josephson. (2010) Neurovascular Complications of Cocaine Use at a Tertiary Stroke Center. Journal of Stroke and Cerebrovascular Diseases 19:4, 273-278
CrossRef11
S. Geibprasert, M. Gallucci, T. Krings. (2010) Addictive Illegal Drugs: Structural Neuroimaging. American Journal of Neuroradiology 31:5, 803-808
CrossRef12
Markus Stenner, Konrad Stürmer, Dirk Beutner, Jens Peter Klussmann. (2009) Sudden bilateral sensorineural hearing loss after intravenous cocaine injection: A case report and review of the literature. The Laryngoscope 119:12, 2441-2443
CrossRef13
M. Boentert, J. Kraus, S. Kloska, R. Dittrich, D. G. Nabavi, T. Niederstadt, E. B. Ringelstein, R. Kiefer. (2009) Obliterating intracranial vasculopathy mimicking multiple sclerosis. Acta Neurologica Scandinavica 120:1, 68-71
CrossRef14
Carlos S. Restrepo, Carlos A. Rojas, Santiago Martinez, Roy Riascos, Alejandro Marmol-Velez, Jorge Carrillo, Daniel Vargas. (2009) Cardiovascular complications of cocaine: Imaging findings. Emergency Radiology 16:1, 11-19
CrossRef15
Tatjana Rundek, Ralph L. Sacco. (2008) Risk Factor Management to Prevent First Stroke. Neurologic Clinics 26:4, 1007-1045
CrossRef16
Clare MacEwen, Mike Ward, Alastair Buchan. (2008) A case of cocaine-induced basilar artery thrombosis. Nature Clinical Practice Neurology 4:11, 622-626
CrossRef17
Patrick C. Hsieh, Issam A. Awad, Christopher C. Getch, Bernard R. Bendok, Szymon S. Rosenblatt, H. Hunt Batjer. (2008) Current Updates in Perioperative Management of Intracerebral Hemorrhage. Neurosurgery Clinics of North America 19:3, 401-414
CrossRef18
Prasad Vannemreddy, Gloria Caldito, Brian Willis, Anil Nanda. (2008) Influence of cocaine on ruptured intracranial aneurysms: a case control study of poor prognostic indicators. Journal of Neurosurgery 108:3, 470-476
CrossRef19
James P. Rathmell, Christopher M. Viscomi, Marjorie Meyer. 2008. Managing Pain during Pregnancy and Lactation. , 565-584.
CrossRef20
M E Couce, R Medina-Flores, M Wong, C T Chu. (2007) Occult germ cell tumour presenting as spontaneous intracerebral haemorrhage. Histopathology 50:6, 789-793
CrossRef21
Karen I. Bolla, Jean Lud Cadet. 2007. Exogenous Acquired Metabolic Disorders of the Nervous System. , 865-896.
CrossRef22
Fred Rincon, Andres Fernandez, Stephan A. Mayer. 2007. Hematologic Interventions for Acute Central Nervous System Disease. , 691-703.
CrossRef23
John C.M. Brust. 2007. Cocaïne. , 171-243.
CrossRef24
Charles Wetli. 2006. Pathology of Drug Abuse. , 71-145.
CrossRef25
Patrick C. Hsieh, Issam A. Awad, Christopher C. Getch, Bernard R. Bendok, Szymon S. Rosenblatt, H. Hunt Batjer. (2006) Current Updates in Perioperative Management of Intracerebral Hemorrhage. Neurologic Clinics 24:4, 745-764
CrossRef26
R Loch Macdonald. (2005) Thrombolysis for Intraventricular Hemorrhage. Neurosurgery Quarterly 15:4, 211-222
CrossRef27
Ayrn D. O'Connor, Daniel E. Rusyniak, Askiel Bruno. (2005) Cerebrovascular and Cardiovascular Complications of Alcohol and Sympathomimetic Drug Abuse. Medical Clinics of North America 89:6, 1343-1358
CrossRef28
Andra H. James, Cheryl D. Bushnell, Margaret G. Jamison, Evan R. Myers. (2005) Incidence and Risk Factors for Stroke in Pregnancy and the Puerperium. Obstetrics & Gynecology 106:3, 509-516
CrossRef29
Bankole A Johnson, Michael A Dawes, John D Roache, Lynda T Wells, Nassima Ait-Daoud, James B Mauldin, Yanmei Wang, Jack L Lancaster, Peter T Fox. (2005) Acute intravenous low- and high-dose cocaine reduces quantitative global and regional cerebral blood flow in recently abstinent subjects with cocaine use disorder. Journal of Cerebral Blood Flow & Metabolism 25:7, 928-936
CrossRef30
Rafael Rojas, Roy Riascos, Daniel Vargas, Hugo Cuellar, Jessica Borne. (2005) Neuroimaging in Drug and Substance Abuse Part I. Topics in Magnetic Resonance Imaging 16:3, 231-238
CrossRef31
(2005) Cocaine and Subarachnoid Hemorrhage. Journal of Neurosurgery 102:5,
CrossRef32
Keyvan Nicoucar, Ken Sakbani, Savo Vukanovic, Jean-Philippe Guyot. (2005) Intralabyrinthine haemorrhage following cocaine consumption. Acta Oto-laryngologica 125:8, 899-901
CrossRef33
I.M. Devonshire, J. Berwick, M. Jones, J. Martindale, D. Johnston, P.G. Overton, J.E.W. Mayhew. (2004) Haemodynamic responses to sensory stimulation are enhanced following acute cocaine administration. NeuroImage 22:4, 1744-1753
CrossRef34
D Ogunyemi, GE Hernández-Loera. (2004) The impact of antenatal cocaine use on maternal characteristics and neonatal outcomes. Journal of Maternal-Fetal and Neonatal Medicine 15:4, 253-259
CrossRef35
Thomas R Kosten, Karen Tucker, P.Christopher Gottschalk, Christine S Rinder, Henry M Rinder. (2004) Platelet abnormalities associated with cerebral perfusion defects in cocaine dependence. Biological Psychiatry 55:1, 91-97
CrossRef36
Carlos S. Kase, J.P. Mohr, Louis R. Caplan. 2004. Intracerebral Hemorrhage. , 327-376.
CrossRef37
John C.M. Brust. 2004. Stroke and Substance Abuse. , 725-745.
CrossRef38
Russel S. Falck, Jichuan Wang, Harvey A. Siegal, Robert G. Carlson. (2003) Current Physical Health Problems and their Predictors Among a Community Sample of Crack-Cocaine Smokers in Ohio. Journal of Psychoactive Drugs 35:4, 471-478
CrossRef39
Jay U. Howington, Scott C. Kutz, Gregory E. Wilding, Deepak Awasthi. (2003) Cocaine use as a predictor of outcome in aneurysmal subarachnoid hemorrhage. Journal of Neurosurgery 99:2, 271-275
CrossRef40
John C.M. Brust. 2003. Drug Dependence. , 1277-1282.
CrossRef41
Askiel Bruno. (2003) Cerebrovascular complications of alcohol and sympathomimetic drug abuse. Current Neurology and Neuroscience Reports 3:1, 40-45
CrossRef42
Carlos S. Kase, Conrado J. Estol. 2003. Intracerebral Hemorrhage. , 315-323.
CrossRef43
Nalini Samuel, Luis D'Olhaberriague, Steven R. Levine, Lawrence M. Brass. 2003. Illicit Drugs and Stroke. , 359-362.
CrossRef44
Esther Cubo, Christopher G. Goetz. 2003. Cocaine. , 733-734.
CrossRef45
John C. M. Brust. (2002) Neurologic Complications of Substance Abuse. JAIDS Journal of Acquired Immune Deficiency Syndromes 31, S29-S34
CrossRef46
(2001) Cardiovascular Complications of Cocaine Use. New England Journal of Medicine 345:21, 1575-1576
Full Text47
J. O'Neill, V. A. Cardenas, D. J. Meyerhoff. (2001) Separate and interactive effects of cocaine and alcohol dependence on brain structures and metabolites: quantitative MRI and proton MR spectroscopic imaging. Addiction Biology 6:4, 347-361
CrossRef48
M Daras. (2001) Bilateral symmetrical basal ganglia infarction after intravenous use of cocaine and heroin. Clinical Imaging 25:1, 12-14
CrossRef49
J. Neiman, H. M. Haapaniemi, M. Hillbom. (2000) Neurological complications of drug abuse: pathophysiological mechanisms. European Journal of Neurology 7:6, 595-606
CrossRef50
Thomas Ernst, Linda Chang, Grace Oropilla, Andrew Gustavson, Oliver Speck. (2000) Cerebral perfusion abnormalities in abstinent cocaine abusers: a perfusion MRI and SPECT study. Psychiatry Research: Neuroimaging 99:2, 63-74
CrossRef51
James M. Gebel, Joseph P. Broderick. (2000) INTRACEREBRAL HEMORRHAGE. Neurologic Clinics 18:2, 419-438
CrossRef52
Gianluca La Monaca, Anthony Donatelli, Jack L Katz. (1999) A Case of Mutism Subsequent to Cocaine Abuse. Journal of Substance Abuse Treatment 17:1-2, 109-112
CrossRef53
George Bartzokis, Mace Beckson, Darwood B Hance, Po H Lu, Jennifer A Foster, Jim Mintz, Walter Ling, Peter Bridge. (1999) Magnetic resonance imaging evidence of “silent” cerebrovascular toxicity in cocaine dependence. Biological Psychiatry 45:9, 1203-1211
CrossRef54
Philip E. Stieg, Carlos S. Kase. (1998) INTRACRANIAL HEMORRHAGE: DIAGNOSIS AND EMERGENCY MANAGEMENT. Neurologic Clinics 16:2, 373-390
CrossRef55
John C.M. Brust. (1998) ACUTE NEUROLOGIC COMPLICATIONS OF DRUG AND ALCOHOL ABUSE. Neurologic Clinics 16:2, 503-519
CrossRef56
Linda Chang, C. Mark Mehringer, Thomas Ernst, Rosemarie Melchor, Hector Myers, David Forney, Paul Satz. (1997) Neurochemical alterations in asymptomatic abstinent cocaine users: A proton magnetic resonance spectroscopy study. Biological Psychiatry 42:12, 1105-1114
CrossRef57
James P. Rathmell, Christopher M. Viscomi, Michael A. Ashburn. (1997) Management of Nonobstetric Pain During Pregnancy and Lactation. Anesthesia & Analgesia 85:5, 1074-1087
CrossRef58
Jenny T. Mao, Li X. Zhu, Sherven Sharma, Ken Chen, Min Huang, S.Jonah Santiago, Jena Gulsurd, Donald P. Tashkin, Steven M. Dubinett. (1997) Cocaine Inhibits Human Endothelial Cell IL-8 Production: The Role of Transforming Growth Factor-β. Cellular Immunology 181:1, 38-43
CrossRef59
David G. Silverman, Thomas R. Kosten, Peter I. Jatlow, Viorel Gutter, Julia Fleming, Theresa Z. OʼConnor, Robert Byck. (1997) Decreased Digital Flow Persists After the Abatement of Cocaine-Induced Hemodynamic Stimulation. Anesthesia & Analgesia 84:1, 46-50
CrossRef60
J Hollander. (1996) Complications from the use of thrombolytic agents in patients with cocaine associated chest pain. Journal of Emergency Medicine 14:6, 731-736
CrossRef61
Frank LoVecchio, Lewis Nelson. (1996) Intraventricular bleeding after the use of thrombolytics in a cocaine user. The American Journal of Emergency Medicine 14:7, 663-664
CrossRef62
C Lucas, D Deplanque, A Salhi, E Hachulla, S Doumith. (1996) Angiopathie bénigne du post-partum: un cas clinicoradiologique associé à la prise de bromocriptine. La Revue de Médecine Interne 17:10, 839-841
CrossRef63
Barbara S. Koppel, Lawrence Samkoff, Michael Daras. (1996) Relation of Cocaine Use to Seizures and Epilepsy. Epilepsia 37:9, 875-878
CrossRef64
Conrad R. Chao. (1996) Cardiovascular effects of cocaine during pregnancy. Seminars in Perinatology 20:2, 107-114
CrossRef65
Kenneth Tardiff, Peter M. Marzuk, Andrew C. Leon, Laura Portera, Nancy Hartwell, Charles S. Hirsch, Marina Stajic. (1996) Accidental Fatal Drug Overdoses in New York City: 1990–1992. The American Journal of Drug and Alcohol Abuse 22:2, 135-146
CrossRef66
Peter A. Merkel, Walter J. Koroshetz, Michael C. Irizarry, Merit E. Cudkowicz. (1995) Cocaine-associated cerebral vasculitis. Seminars in Arthritis and Rheumatism 25:3, 172-183
CrossRef67
M Strobel, I Lamaury, F Brouzes, C Léonardi, B Dorak, M.T. Sow, S Pelczar, S Roul, F Cnudde, J.M. Gabriel. (1995) Accidents vasculaires cérébraux et sida. La Revue de Médecine Interne 16:10, 743-746
CrossRef68
Marzuk, Peter M., Tardiff, Kenneth, Leon, Andrew C., Hirsch, Charles S., Stajic, Marina, Portera, Laura, Hartwell, Nancy, Iqbal, M. Irfan, . (1995) Fatal Injuries after Cocaine Use as a Leading Cause of Death among Young Adults in New York City. New England Journal of Medicine 332:26, 1753-1757
Full Text69
Brian K. Iriye, Tamerou Asrat, Joseph A. Adashek, Margaret H. Carr. (1995) Intraventricular haemorrhage and maternal brain death associated with antepartum cocaine abuse. BJOG: An International Journal of Obstetrics and Gynaecology 102:1, 68-69
CrossRef70
O'Connor, Patrick G.Selwyn, Peter A.Schottenfeld, Richard S.. (1994) Medical Care for Injection-Drug Users with Human Immunodeficiency Virus Infection. New England Journal of Medicine 331:7, 450-459
Full Text71
Maria Luiza C. Albuquerque, C. Dean Kurth. (1993) Cocaine constricts immature cerebral arterioles by a local anesthetic mechanism. European Journal of Pharmacology 249:2, 215-220
CrossRef72
Michels, RobertMarzuk, Peter M.. (1993) Progress in Psychiatry. New England Journal of Medicine 329:9, 628-638
Full Text73
Cabot, Richard C.Scully, Robert E., Mark, Eugene J., McNeely, William F., McNeely, Betty U., Tapia, Jorge F.Schumacher, James M.. (1993) Case 27-1993. New England Journal of Medicine 329:2, 117-124
Full Text74
Leonard Handelsman, In Sook Song, Miklos Losonczy, Sun Park, Jeffrey Jacobson, Jill Wiener, Marvin Aronson. (1993) Magnetic resonance abnormalities in HIV infection: A study in the drug-user risk group. Psychiatry Research 47:2, 175-186
CrossRef75
J. S. Fowler, N. D. Volkow, J. Logan, R. R. MacGregor, G.-J. Wang, A. P. Wolf. (1992) Alcohol inoxication does not change [11C]cocaine pharmacokinetics in human brain and heart. Synapse 12:3, 228-235
CrossRef76
H. Virginia McCoy, Christine Miles. (1992) A Gender Comparison of Health Status Among Users of Crack Cocaine. Journal of Psychoactive Drugs 24:4, 389-397
CrossRef77
Anil Dhuna, Alvaro Pascual-Leone, Frederick Langendorf. (1991) Chronic, Habitual Cocaine Abuse and Kindling-Induced Epilepsy: A Case Report. Epilepsia 32:6, 890-894
CrossRef78
Jean Paul G. Vonsattel, Richard H. Myers, E. Tessa Hedley-Whyte, Allan H. Ropper, Edward D. Bird, Edward P. Richardson. (1991) Cerebral amyloid angiopathy without and with cerebral hemorrhages: A comparative histological study. Annals of Neurology 30:5, 637-649
CrossRef79
Wendy Chavkin, Machelle Harris Allen, Michelle Oberman. (1991) Drug Abuse and Pregnancy: Some Questions on Public Policy, Clinical Management, and Maternal and Fetal Rights. Birth 18:2, 107-112
CrossRef80
Eelco F. M. Wijdicks, Jan C. C. Borleffs, Andy I. M. Hoepelman, Gerard H. Jansen. (1991) Fatal disseminated hemorrhagic toxoplasmic encephalitis as the initial manifestation of AIDS. Annals of Neurology 29:6, 683-686
CrossRef
