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viernes, 25 de noviembre de 2011

violence video games

Estimado Dr Hernández Guevara y miembros de las listas:

      Van 20 artículos sobre videojuegos de violencia.
      El primer artículo esta interesantísimo, es sobre el efecto del video juego
violento en la corteza orbito-frontal, según los autores de este trabajo la
substancia gris se reduce en esta zona del cerebro, específicamente en la
corteza orbito-frontal izquierda.

     Aquí surge la pregunta de si los niños o adolescentes de este grupo
estudiado ya estaban con estos cambios morfológicos, o si el tipo de actividad
desencadenó estos cambios. La pregunta podría ser relevante porque sería
posible que con este tipo de actividad estemos generando en algunos
grupos de la población suscepibles, muchas personalidades con rasgos sociopáticos.

    ¿Que opinan?

saludos cordiales,
Gustavo

----- Forwarded Message -----
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To: jgustavo@yahoo.com
Sent: Friday, November 25, 2011 9:20 PM
Subject: PMC Search Results

This message contains search results from the National Center for Biotechnology Information at the U.S. National Library of Medicine. Do not reply directly to this message
Sender's message: violence video games
Sent on: Fri Nov 25 22:15:25 2011
Search: violence video games


PMC Results
Items 1 - 20 of 116

1.
Kevin Haninger, M. Seamus Ryan, Kimberly M Thompson
MedGenMed. 2004; 6(1): 1. Published online 2004 March 12.
PMCID:
PMC1140725
2.
Heidi M. Zinzow, Kenneth J. Ruggiero, Rochelle F. Hanson, Daniel W. Smith, Benjamin E. Saunders, Dean G. Kilpatrick
J Trauma Stress. Author manuscript; available in PMC 2010 December 1.
Published in final edited form as: J Trauma Stress. 2009 December; 22(6): 525–533. doi: 10.1002/jts.20469
PMCID:
PMC2798911
3.
Deepa Natarajan, Doretta Caramaschi
Front Behav Neurosci. 2010; 4: 9. Prepublished online 2009 September 11. Published online 2010 April 5. doi: 10.3389/fnbeh.2010.00009
PMCID:
PMC2854525
4.
Ryan C. W. Hall, Terri Day, Richard C. W. Hall
Mayo Clin Proc. 2011 April; 86(4): 315–321. doi: 10.4065/mcp.2010.0762
PMCID:
PMC3068891
5.
L. Rowell Huesmann
Psychol Bull. Author manuscript; available in PMC 2011 March 1.
Published in final edited form as: Psychol Bull. 2010 March; 136(2): 179–181. doi: 10.1037/a0018567
PMCID:
PMC2848956
6.
L. Rowell Huesmann
J Adolesc Health. Author manuscript; available in PMC 2009 June 30.
Published in final edited form as: J Adolesc Health. 2007 December; 41(6 Suppl 1): S6–13. doi: 10.1016/j.jadohealth.2007.09.005
PMCID:
PMC2704015
7.
Erin C. Hastings, Tamara L. Karas, Adam Winsler, Erin Way, Amy Madigan, Shannon Tyler
Issues Ment Health Nurs. Author manuscript; available in PMC 2011 February 18.
Published in final edited form as: Issues Ment Health Nurs. 2009 October; 30(10): 638–649. doi: 10.1080/01612840903050414
PMCID:
PMC3041171
8.
Frederick W Kron, Craig L Gjerde, Ananda Sen, Michael D Fetters
BMC Med Educ. 2010; 10: 50. Published online 2010 June 24. doi: 10.1186/1472-6920-10-50
PMCID:
PMC2908629
9.
Douglas A. Gentile, Craig A. Anderson, Shintaro Yukawa, Nobuko Ihori, Muniba Saleem, Lim Kam Ming, Akiko Shibuya, Albert K. Liau, Angeline Khoo, Brad J. Bushman, L. Rowell Huesmann, Akira Sakamoto
Pers Soc Psychol Bull. Author manuscript; available in PMC 2009 June 1.
Published in final edited form as: Pers Soc Psychol Bull. 2009 June; 35(6): 752–763. Published online 2009 March 25. doi: 10.1177/0146167209333045
PMCID:
PMC2678173
10.
Kimberly M Thompson, Fumie Yokota
MedGenMed. 2004; 6(3): 3. Published online 2004 July 12.
PMCID:
PMC1435631
11.
Keilah A. Worth, Jennifer Gibson Chambers, Daniel H. Nassau, Balvinder K. Rakhra, James D. Sargent
Pediatrics. Author manuscript; available in PMC 2009 November 17.
Published in final edited form as: Pediatrics. 2008 August; 122(2): 306–312. doi: 10.1542/peds.2007-1096
PMCID:
PMC2778277
12.
Philip A Chan, Terry Rabinowitz
Ann Gen Psychiatry. 2006; 5: 16. Published online 2006 October 24. doi: 10.1186/1744-859X-5-16
PMCID:
PMC1635698
13.
Hamid Allahverdipour, Mohsen Bazargan, Abdollah Farhadinasab, Babak Moeini
BMC Public Health. 2010; 10: 286. Published online 2010 May 27. doi: 10.1186/1471-2458-10-286
PMCID:
PMC2894772
14.
Maren Strenziok, Frank Krueger, Sarah J. Pulaski, Anne E. Openshaw, Giovanna Zamboni, Elke van der Meer, Jordan Grafman
J Adolesc Health. Author manuscript; available in PMC 2011 June 1.
Published in final edited form as: J Adolesc Health. 2010 June; 46(6): 607–609. Published online 2010 January 13. doi: 10.1016/j.jadohealth.2009.11.196
PMCID:
PMC2872635
15.
George Spears, Kasia Seydegart
Can Child Adolesc Psychiatr Rev. 2004 February; 13(1): 7–12.
PMCID:
PMC2533815
16.
Maxine M. Denniston, Monica H. Swahn, Marci Feldman Hertz, Lisa M. Romero
West J Emerg Med. 2011 July; 12(3): 310–315.
PMCID:
PMC3117607
17.
John Zarocostas
BMJ. 2006 October 21; 333(7573): 822. doi: 10.1136/bmj.333.7573.822-b
PMCID:
PMC1618462
18.
Daniel S. Schechter, Anna Gross, Erica Willheim, Jaime McCaw, J. Blake Turner, Michael M. Myers, Charles H. Zeanah, Mary Margaret Gleason
J Trauma Stress. Author manuscript; available in PMC 2010 December 1.
Published in final edited form as: J Trauma Stress. 2009 December; 22(6): 658–662. doi: 10.1002/jts.20472
PMCID:
PMC2798921
19.
Geoffrey L. Ream, Luther C. Elliott, Eloise Dunlap
Int J Environ Res Public Health. 2011 October; 8(10): 3979–3998. Published online 2011 October 18. doi: 10.3390/ijerph8103979
PMCID:
PMC3210592
20.
Jeroen S. Lemmens, Patti M. Valkenburg, Jochen Peter
J Youth Adolesc. 2011 January; 40(1): 38–47. Published online 2010 June 13. doi: 10.1007/s10964-010-9558-x
PMCID:
PMC3003785




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lunes, 21 de noviembre de 2011

CIRUGIA EXPERIMENTAL: SISTEMAS DE DERIVACION DE FLUJO CONTINUO

LOS CORREOS ABAJO  EXPUESTOS CORRESPONDEN
 ACTUALMENTE AL DEBATE QUE SE ESTA DANDO EN
LA COMUNIDAD VIRTUAL DE NEUROCIENCIAS EN
RELACIÓN A LA LLAMADA  CIRUGIA EXPERIMENTAL
 DE COLOCACION  DE SISTEMAS DE DERIVACION DE
FLUJO CONTINUO. LOS COMENTARIOS AQUI VERTIDOS
NO TIENEN VALIDEZ LEGAL, NI VALOR DE PRUEBA,
AUNQUE PUEDAN  EXPRESAR OPINIONES, HECHOS
 O JUICIOS CONTRADICTORIOS EN RELACION
 A LA HISTORIA DE ESTE MUY CUESTIONADO
 PROCEDIMIENTO.

EL ADMINISTRADOR DEL BLOG

DR. J GUSTAVO VEGA GAMA


----- Original Message -----


From: Faustino Llamas Ibarra

Sent: 11/19/11 07:20 AM

To: AMEINNN GOOGLEGROUPS

Subject: RE: [ameinnn:3749] "googleando" escándalos internacionales


Para Rodolfo y Arturo, respectivamente.

Rodolfo:

Disculpa que no te conteste com anterioridad,  estoy muy ocupado,  ahora te comento:

1.- Las, aproximadamente 37 cirugías de derivación ventrículo peritoneal se realizaron en la Clínica Neurológica de Querétaro.

2.- En cuanto a las fechas en que he operado estos pacientes, te puedo decir que han sido los últimos 6 años. Hasta el momento, en mi experiencia, es una opción que funciona.

3.-  En lo referente al grupo de edad,  con excepción de una paciente pediátrica (disfuncionó, lo comenté con el Dr. Sotelo y me dijo que, efectivamente, este sistema no es adecuado en edad pediátrica), todos los pacientes son adultos, no tengo las edades exactas ya que nunca pretendí  hacer investigación sobre lo que, con una gran casuística, lo hacían en el INNNMVS.

4.-  Preguntas quién envió los sistemas: el Dr. Sotelo

5.-  Cuántos envíos ha habido: tal vez uno cada 6 meses, le llaman por teléfono (el jefe de almacén) y nos mandan,  generalmente,  5 válvulas.

6.- Hasta donde yo sé, los envían por Estafeta con porte pagado.

7.- Las fechas de los envíos no las sé.

8.- No hubo costo para los pacientes porque, como comenté, el Dr. Sotelo me envía gratuitamente los sistemas.

Ahora, el punto central, en mi opinión es el siguiente:

Afirman 500 procedimientos, 350 muertos. ¡Increíble!

......

Con el gusto de siempre los saludo. Su amigo. Faustino.
------------------------------------------------------------------------------------------------------------



Estimad@s miembros de la AMEINNN,
¿Qué es lo que dice la CONAMED con respecto a la cirugía experimental ilegal realizada en el Instituto Nacional de Neurología y Neurocirugía, Ciudad de México?
Pues entre otras cosas se afirma lo siguiente:

La Comisión Nacional de Arbitraje Médico (CONAMED): "Ahora bien, en relación al sistema de derivación ventricular de flujo libre (sin mecanismo valvular), desarrollado en el INNN, no es un dispositivo con autorización sanitaria para su empleo en seres humanos… el INNN no debe utilizarlo en la atención ordinaria de los pacientes….no debía ser utilizado a menos que existiera un protocolo de investigación vigente autorizado y previo consentimiento bajo información suscrito ...en los términos señalados en la Ley General de Salud y su Reglamento en Materia de Investigación para la Salud. En la especie, no se acredita que esto haya sucedido… A mayor abundamiento, requería, además, ajustarse a las disposiciones de los artículos 61, 62, 73 y 113 del Reglamento de Referencia…Tratándose de un dispositivo sin registro sanitario, además, debió solicitarse el consentimiento bajo información, atendiendo a las disposiciones normativas contenidas en los artículos 20, 21 y 22 del Reglamento de la Ley General de Salud en materia de Investigación para la Salud…En estos términos, apreciamos mal praxis del personal administrativo del Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", al permitir el empleo de un dispositivo en fase de investigación como un recurso de atención médica ordinaria. En la especie no se observaron las disposiciones de la Ley General de Salud y su Reglamento en materia de Investigación para la Salud." (sic).
En el mismo documento se aclara que también fueron violadas diversas Normas Oficiales Mexicanas e internacionales (especificaciones sanitarias de los equipos para derivación de líquido cefalorraquídeo NOM-098-SSA1-1994 e ISO 7197, Proyecto de Norma Oficial Mexicana PROY-NOM-012-SSA3-2007, que establece los criterios para la ejecución de proyectos de investigación para la salud en seres humanos).
Corroborando la información previa, la Comisión Federal para la Protección Contra Riesgos Sanitarios (COFEPRIS) ha afirmado: "no ha expedido ningún Registro Sanitario con el nombre del producto Sistema de Derivación Ventrículo Peritoneal tipo INNN (SDVP INNN PCD)".
Respetuosamente
Dr. Rodolfo Ondarza Rovira

----------------------------------------------------------------------------------------------------------


>> Estimad@s miembros de la AMEINNN,
>>
>> Este es uno de los puntos de acuerdo presentados ante la Cámara de Diputados. Existe otro presentado por el Senador González Yañez, y el último por el Senador Ricardo Monreal (uno de los aspirantes al Gobierno del D. F.)

Jueves, 15 de marzo de 2007

Gaceta Parlamentaria, año X, número 2214

 

Con punto de acuerdo, por el que se solicita a la ASF que realice una auditoría al Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, a cargo del diputado Ricardo Cantú Garza, del Grupo Parlamentario del Partido del Trabajo. (Turno a Comisión)

 

 

"Recientemente se entregó el Premio al Mérito Médico al señor Julio Everardo Sotelo Morales, que es un reconocimiento al gremio médico por parte del gobierno federal. La recepción de este premio no generaría polémica de no ser por la persona a quien se otorgó, porque se trata de un personaje que se ha dedicado a hacer de la medicina experimental un modus operandi para ganar fama a costa de poner en riesgo la vida de los pacientes, tal como consta en las denuncias de hechos ante el Ministerio Público, que han sido presentadas por los afectados, quienes fueron utilizados como conejillos de indias, sin su consentimiento."
 

 

 

http://gaceta.diputados.gob.mx/Gaceta/60/2007/mar/20070315.html

 

 

http://sil.gobernacion.gob.mx/Archivos/Documentos/2007/04/asun_2341404_20070426_1179846997.pdf


Respetuosamente

Dr. Rodolfo Ondarza

------------------------------------------------------------------------------------------------------------------




 

 

 









COCAINE + STROKE

Querido ahijado (Alejandro Mendez jr)

       Aquí esta lo que me pediste a propósito del caso que me comentaste, espero que se de utilidad,
hay algunos artículos que no tienen relevancia clínica, pero otros que te puedan dar una orientación
de como abordar el problema, son de texto completo y acceso libre.

      Lo  mando también a nuestra comunidad virtual. Asi se aprende, caso que veo, caso que me remito
a estudiar e investigar.

     Un saludo cordial,

Gustavo

This message contains search results from the National Center for Biotechnology Information at the U.S. National Library of Medicine. Do not reply directly to this message
Sender's message: PALABRAS CLAVE: STROKE + COCAINE
Sent on: Mon Nov 21 10:27:38 2011
Search: (#6) AND #7


PubMed Results
Items 1 - 21 of 83

1. Rev Neurol. 2010 Jan 16-31;50(2):126-7.

[Ischemic stroke associated with the consumption of cocaine].

[Article in Spanish]
Rodríguez-Gómez D, Mouriño-López Y, Marnotes-González J.

Source

Complexo Hospitalario de Ourense, Ourense, Espana. diegorg1958@gmail.com
Free Article
PMID:
20112221
[PubMed - indexed for MEDLINE]
Related citations
Click here to read

2. Stroke. 2009 Nov;40(11):3635-7. Epub 2009 Sep 10.

Intravenous tissue plasminogen activator in patients with cocaine-associated acute ischemic stroke.

Martin-Schild S, Albright KC, Misra V, Philip M, Barreto AD, Hallevi H, Grotta JC, Savitz SI.

Abstract

BACKGROUND AND PURPOSE:

The safety of thrombolytic therapy in patients with cocaine-associated acute ischemic stroke (CIS) is unknown.

METHODS:

We conducted a retrospective review of patients with CIS who presented to our stroke center. Thrombolytic treatment was compared between cocaine-positive (n=29) and cocaine-negative (n=75) patients. We also compared patients with CIS treated with tissue plasminogen activator versus those who did not receive tissue plasminogen activator (n=58). Safety outcomes were determined by the incidence of symptomatic intracerebral hemorrhage, in-hospital mortality, and modified Rankin Scale at hospital discharge.

RESULTS:

There were no complications in tissue plasminogen activator-treated patients with CIS. Cocaine-positive and cocaine-negative treated patients had similar stroke severity and safety outcomes. Patients with CIS treated with tissue plasminogen activator had more severe strokes on baseline National Institutes of Health Stroke Scale but similar safety outcomes compared with nontreated patients with CIS.

CONCLUSIONS:

Thrombolytic therapy for CIS appears to be safe in this small study. Further research is needed to more definitively assess safety and efficacy of tissue plasminogen activator for CIS.
Free Article
PMID:
19745181
[PubMed - indexed for MEDLINE]
Related citations
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3. Pharmacol Ther. 2009 Nov;124(2):195-206. Epub 2009 Jul 18.

The pharmacology of sigma-1 receptors.

Maurice T, Su TP.

Source

Team II Endogenous Neuroprotection in Neurodegenerative Diseases, INSERM U. 710, 34095 Montpellier Cedex 5, France. Tangui.Maurice@univ-montp2.fr

Abstract

Originally considered an enigmatic protein, the sigma-1 receptor has recently been identified as a unique ligand-regulated molecular chaperone in the endoplasmic reticulum of cells. This discovery causes us to look back at the many proposed roles of this receptor, even before its molecular function was identified, in many diseases such as methamphetamine or cocaine addiction, amnesia, pain, depression, Alzheimer's disease, stroke, retinal neuroprotection, HIV infection, and cancer. In this review, we examine the reports that have clearly shown an agonist-antagonist relationship regarding sigma-1 receptors in models of those diseases and also review the relatively known mechanisms of action of sigma-1 receptors in an attempt to spur the speculation of readers on how the sigma-1 receptor at the endoplasmic reticulum might relate to so many diseases. We found that the most prominent action of sigma-1 receptors in biological systems including cell lines, primary cultures, and animals is the regulation and modulation of voltage-regulated and ligand-gated ion channels, including Ca(2+)-, K(+)-, Na(+), Cl(-), and SK channels, and NMDA and IP3 receptors. We found that the final output of the action of sigma-1 receptor agonists is to inhibit all above-mentioned voltage-gated ion channels, while they potentiate ligand-gated channels. The inhibition or potentiation induced by agonists is blocked by sigma-1 receptor antagonists. Other mechanisms of action of sigma-1 receptors, and to some extent those of sigma-2 receptors, were also considered. We conclude that the sigma-1 and sigma-2 receptors represent potential fruitful targets for therapeutic developments in combating many human diseases.
PMCID: PMC2785038
Free PMC Article
PMID:
19619582
[PubMed - indexed for MEDLINE]
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4. Neuroscience. 2008 Apr 9;152(4):1040-53. Epub 2008 Feb 7.

Inhibiting activator protein-1 activity alters cocaine-induced gene expression and potentiates sensitization.

Paletzki RF, Myakishev MV, Polesskaya O, Orosz A, Hyman SE, Vinson C.

Source

Laboratory of Molecular Pathophysiology, National Institute of Neurological Disorders and Stroke, NIH, Building 36, Room 4C-24, Bethesda, MD 20892, USA.

Abstract

We have expressed A-FOS, an inhibitor of activator protein-1 (AP-1) DNA binding, in adult mouse striatal neurons. We observed normal behavior including locomotion and exploratory activities. Following a single injection of cocaine, locomotion increased similarly in both the A-FOS expressing and littermate controls. However, following repeated injections of cocaine, the A-FOS expressing mice showed increased locomotion relative to littermate controls, an increase that persisted following a week of withdrawal and subsequent cocaine administration. These results indicate that AP-1 suppresses this behavioral response to cocaine. We analyzed mRNA from the striatum before and 4 and 24 h after a single cocaine injection in both A-FOS and control striata using Affymetrix microarrays (430 2.0 Array) to identify genes mis-regulated by A-FOS that may mediate the increased locomotor sensitization to cocaine. A-FOS expression did not change gene expression in the basal state or 4 h following cocaine treatment relative to controls. However, 24 h after an acute cocaine treatment, 84 genes were identified that were differentially expressed between the A-FOS and control mice. Fifty-six genes are down-regulated while 28 genes are up-regulated including previously identified candidates for addiction including brain-derived neurotrophic factor and period homolog 1. Using a random sample of identified genes, quantitative PCR was used to verify the microarray studies. The chromosomal location of these 84 genes was compared with human genome scans of addiction to identify potential genes in humans that are involved in addiction.
PMCID: PMC2585517
Free PMC Article
PMID:
18355967
[PubMed - indexed for MEDLINE]
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5. J Invasive Cardiol. 2007 Dec;19(12):E378-80.

Transient left ventricular apical ballooning after a cocaine binge.

Daka MA, Khan RS, Deppert EJ.

Source

St. Luke's-Roosevelt Hospital Center, University Hospital of Columbia University College of Physicians and Surgeons, 1111 Amsterdam Avenue, New York, NY 10025, USA. mattmdmd@gmail.com

Abstract

Left ventricular apical ballooning is an increasingly reported phenomenon with an onset that is usually triggered by severe and often acute emotional incidents. We report a rare case of acute left ventricular apical ballooning syndrome, mimicking acute ST-elevation myocardial infarction, in a post menopausal woman whose only predisposing factor was an all-night cocaine binge.
Free Article
PMID:
18180533
[PubMed - indexed for MEDLINE]
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6. Postgrad Med J. 2007 Jun;83(980):389-94.

Cocaine use and stroke.

Treadwell SD, Robinson TG.

Source

Department of Integrated Medicine, University Hospitals of Leicester NHS Trust, Leicester Royal Infirmary, Leicester, UK. seantreadwell@hotmail.com

Abstract

Stroke is the third most common cause of death in developed countries. In England and Wales, 1000 people under the age of 30 have a stroke each year. Cocaine is the most commonly used class A drug, and the first report of cocaine-induced stroke was in 1977. Since the development of alkaloidal "crack" cocaine in the 1980s, there has been a significant rise in the number of case reports describing both ischaemic and haemorrhagic stroke associated with cocaine use. Cocaine is a potent central nervous system stimulant, and acts by binding to specific receptors at pre-synaptic sites preventing the reuptake of neurotransmitters. The exact mechanism of cocaine-induced stroke remains unclear and there are likely to be a number of factors involved including vasospasm, cerebral vasculitis, enhanced platelet aggregation, cardioembolism, and hypertensive surges associated with altered cerebral autoregulation. The evidence surrounding each of these factors will be considered here.
PMCID: PMC2600058
Free PMC Article
PMID:
17551070
[PubMed - indexed for MEDLINE]
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7. Arch Gen Psychiatry. 2007 Apr;64(4):495-502.

Stroke in young adults who abuse amphetamines or cocaine: a population-based study of hospitalized patients.

Westover AN, McBride S, Haley RW.

Source

Department of Psychiatry, Division of Epidemiology and Preventive Medicine, The University of Texas Southwestern Medical Center at Dallas, TX 75390, USA.

Abstract

CONTEXT:

The abuse of stimulant drugs is increasing in the western United States. Although numerous case reports and animal studies suggest a link with stroke, epidemiologic studies have yielded conflicting results.

OBJECTIVE:

To test the hypothesis that young adults who abuse amphetamines or cocaine are at a higher risk of stroke. Design, Setting, and

PARTICIPANTS:

Using a cross-sectional design and from a quality indicators' database of 3 148 165 discharges from Texas hospitals, we estimated the secular trends from January 1, 2000, to December 31, 2003, in the abuse of various drugs and of strokes. We developed separate logistic regression models of risk factors for hemorrhagic (n = 937) and ischemic (n = 998) stroke discharges of persons aged 18 to 44 years in 2003, and for mortality risk in patients with stroke. Main Outcome Measure Incidence of stroke using definitions from the Agency for Healthcare Research and Quality's stroke mortality Inpatient Quality Indicator.

RESULTS:

From 2000 to 2003, the rate of increase was greatest for abuse of amphetamines, followed by cannabis and cocaine. The rate of strokes also increased, particularly among amphetamine abusers. In 812 247 discharges in 2003, amphetamine abuse was associated with hemorrhagic stroke (adjusted odds ratio [OR], 4.95; 95% confidence interval [CI], 3.24-7.55), but not with ischemic stroke; cocaine abuse was associated with hemorrhagic (OR, 2.33; 95% CI, 1.74-3.11) and ischemic (OR, 2.03; 95% CI, 1.48-2.79) stroke. Amphetamine, but not cocaine, abuse was associated with a higher risk of death after hemorrhagic stroke (OR, 2.63; 95% CI, 1.07-6.50).

CONCLUSION:

Increases in stimulant drug abuse may increase the rate of hospital admissions for strokes and stroke-related mortality.
Free Article
PMID:
17404126
[PubMed - indexed for MEDLINE]
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8. Postgrad Med J. 2005 Sep;81(959):568-71.

Cocaine and the heart.

Egred M, Davis GK.

Source

Cardiothoracic Centre, Thomas Drive, Liverpool L14 3PE, UK. m.egred@ctc.nhs.uk

Abstract

Cocaine is the second commonest illicit drug used and the most frequent cause of drug related deaths. Its use is associated with both acute and chronic complications that may involve any system, the most common being the cardiovascular system. Cocaine misuse has a major effect in young adult drug users with resulting loss of productivity and undue morbidity with cocaine related cardiac and cerebrovascular effects. Many cocaine users have little or no idea of the risks associated with its use. Patients, health care professionals, and the public should be educated about the dangers and the considerable risks of cocaine use. This review concentrates on the cardiovascular effects of cocaine and their management.
PMCID: PMC1743343
Free PMC Article
PMID:
16143686
[PubMed - indexed for MEDLINE]
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9. Stroke. 2003 Aug;34(8):1859-63. Epub 2003 Jul 3.

Risk factors for continued cigarette use after subarachnoid hemorrhage.

Ballard J, Kreiter KT, Claassen J, Kowalski RG, Connolly ES, Mayer SA.

Source

Division of Critical Care Neurology, Department of Neurology, Columbia University College of Physicians and Surgeons, New York, NY, USA. sam14@columbia.edu

Abstract

BACKGROUND AND PURPOSE:

Cigarette smoking is a risk factor for the formation and rupture of intracranial aneurysms. Few studies have examined predictors of resumption of cigarette smoking after a first episode of subarachnoid hemorrhage (SAH).

METHODS:

Of 620 SAH patients treated between July 1996 and November 2002, we prospectively evaluated continued cigarette use in 152 smokers alive at 3 months. Univariate and multivariate logistic regression analyses were used to identify potential demographic, social, and clinical predictors of continued cigarette use, defined as smoking > or =1 cigarette per week in the month before follow-up.

RESULTS:

Thirty-seven percent (56 of 152) resumed smoking after their SAH. Patients who continued smoking were younger, were more often black, had begun smoking at an earlier age, and had a higher frequency of prior alcohol or cocaine use and self-reported depression or anxiety than those who quit (all P<0.05). Smoking at < or =16 years of age (odds ratio [OR], 5.88; 95% confidence interval [CI], 2.33 to 14.29), self-reported depression (OR, 5.29; 95% CI, 2.10 to 13.35), and prior alcohol use (OR, 4.51; 95% CI, 1.45 to 14.05) independently predicted continued cigarette use. Smokers had a functional outcome similar to that of nonsmokers at 3 months but were more likely to resume alcohol consumption (OR, 3.88; 95% CI, 1.91 to 7.88).

CONCLUSIONS:

More than one third of prior smokers continue to use nicotine after SAH. Young age at smoking onset and a history of depression or alcohol use are risk factors for continued cigarette use. Targeted smoking cessation programs are needed to reduce the high rate of smoking resumption after SAH.
Free Article
PMID:
12843355
[PubMed - indexed for MEDLINE]
Related citations
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10. Stroke. 2003 Jun;34(6):1375-81. Epub 2003 May 22.

Major risk factors for aneurysmal subarachnoid hemorrhage in the young are modifiable.

Broderick JP, Viscoli CM, Brott T, Kernan WN, Brass LM, Feldmann E, Morgenstern LB, Wilterdink JL, Horwitz RI; Hemorrhagic Stroke Project Investigators.

Source

Department of Neurology, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45267, USA. joseph.Broderick@uc.edu

Abstract

BACKGROUND AND PURPOSE:

To identify risk factors for subarachnoid hemorrhage (SAH) and intracerebral hemorrhage, we designed a case-control study of men and women 18 to 49 years of age (the Hemorrhagic Stroke Project [HSP]). This report focuses on SAH.

METHODS:

Patients were recruited from 44 hospitals in the United States. Cases with SAH must have had a ruptured aneurysm documented by angiography or surgery. Two controls, identified by random digit dialing and matched to each patient for age, sex, race, and telephone exchange, were sought for each case subject.

RESULTS:

Between 1994 and 1999, 425 patients with SAH were enrolled in HSP, and 312 cases met the criteria for aneurysmal SAH. The present analyses also included 618 matched controls. Of the 312 cases, 66% were current cigarette smokers compared with 30% of controls (adjusted odds ratio [OR], 3.73; 95% CI, 2.67 to 5.21). Cocaine use within the previous 3-day period was reported by 3% of cases and no controls (bivariate exact OR, 24.97; 95% exact CI, 3.95 to infinity; adjusted estimate not calculable). Other independent risk factors in the multivariable model included hypertension (adjusted OR, 2.21; 95% CI, 1.48 to 3.29), low body mass index (OR, 1.59; 95% CI, 1.08 to 2.35), primary family history of hemorrhagic stroke (OR, 3.83; 95% CI, 1.73 to 8.46), caffeine in pharmaceutical products (OR, 2.48; 95% CI, 1.19 to 5.20), lower educational achievement (OR, 2.36; 95% CI, 1.44 to 3.87), and nicotine in pharmaceutical products (adjusted estimate not calculable).

CONCLUSIONS:

Aneurysmal SAH may be largely a preventable disease among the young and middle-aged because several prevalent risk factors can be modified by medication (eg, hypertension) or behavioral change (eg, cigarette smoking, cocaine use). The association of caffeine and nicotine in pharmaceutical products and aneurysmal SAH warrants further study.
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PMID:
12764233
[PubMed - indexed for MEDLINE]
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11. Stroke. 2002 Jul;33(7):1747-8; author reply 1747-8.

Vascular complications of cocaine use.

Noël B. Free Article
PMID:
12105344
[PubMed - indexed for MEDLINE]
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12. Stroke. 2001 Oct;32(10):2338-43.

Cocaine use is an independent risk factor for cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

Conway JE, Tamargo RJ.

Source

Department of Neurosurgery, Division of Vascular Neurosurgery, The Johns Hopkins Medical Institutions, Baltimore, MD, USA.

Abstract

BACKGROUND AND PURPOSE:

Although acute cocaine use has been temporally associated with aneurysmal subarachnoid hemorrhage (aSAH), the prevalence of vasospasm and the clinical outcome of patients experiencing aSAH associated with cocaine exposure are unclear. We have analyzed this patient population in our institution to address these issues.

METHODS:

Between 1992 and 1999, 440 patients presented to our institution with aSAH. This sample was retrospectively analyzed to determine which patients had used cocaine within 72 hours of aSAH as documented by urine toxicology studies or patient history. These patients were then compared with control aSAH patients without recent cocaine exposure through univariable and multivariable analyses.

RESULTS:

Twenty-seven aSAH patients (6.1% of total) had either urine toxicology positive for cocaine metabolites (20 patients, 74%) or a history of cocaine use within 72 hours of aSAH (7 patients, 26%). Cocaine users were more likely to experience cerebral vasospasm defined as a delayed clinical deficit (from 3 to 16 days after aSAH) unexplained by concurrent CT scan and either responsive to hypervolemic and/or hypertensive therapy or accompanied by angiographic confirmation of vessel narrowing than control subjects (63% versus 30%; odds ratio [OR], 3.90; 95% confidence interval [CI], 1.77 to 8.62; P=0.001). Patients using cocaine were younger than control subjects (mean age, 36 versus 52 years; P<0.0001). Aneurysms of the anterior circulation were observed more frequently in cocaine users than in control subjects (97% versus 84%; OR, 6.89; 95% CI, 1.18 to 47.47; P=0.029). A significant difference was not observed, however, in the discharge Glasgow Outcome Scale (GOS) scores between the 2 groups (P=0.73). Differences were not observed between the 2 groups when the distributions of sex, hypertension, admission Glasgow Coma Scale subarachnoid hemorrhage grade, and multiple aneurysms were analyzed. Logistic regression models identified variables independently associated with vasospasm and discharge GOS score. Only a thick blood clot on the admission CT (OR, 7.46; 95% CI, 3.95 to 14.08; P<0.0001) and recent cocaine use (OR, 6.41; 95% CI, 2.14 to 19.23; P=0.0009) were independently associated with vasospasm. Cocaine use was not independently associated with the discharge GOS score.

CONCLUSIONS:

We conclude that there is an increased prevalence of vasospasm in aSAH patients with recent cocaine exposure but no difference in clinical outcome. In addition, these patients are younger and more likely to have anterior circulation aneurysms.
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PMID:
11588323
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13. Circulation. 2001 Jan 30;103(4):502-6.

Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the Third National Health and Nutrition Examination Survey.

Qureshi AI, Suri MF, Guterman LR, Hopkins LN.

Source

Department of Neurosurgery and Toshiba Stroke Research Center, School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY 14209-1194, USA. aiqureshi@hotmail.com

Abstract

BACKGROUND:

Numerous case series have implicated cocaine use as a cause of both myocardial infarction (MI) and stroke on the basis of the temporal relationship between drug use and event onset. Increasing cocaine use in the US population, especially in younger individuals, mandates a more extensive investigation of this relationship.

METHODS AND RESULTS:

We determined the association of cocaine use with self-reported physician diagnosis of MI or stroke in a nationally representative sample of 10 085 US adults aged 18 to 45 years who participated in the Third National Health and Nutrition Examination Survey. A total of 46 nonfatal MIs and 33 nonfatal strokes were reported. After adjusting for differences in age, sex, race/ethnicity, education, hypertension, diabetes mellitus, cholesterol level, body mass index, and cigarette smoking, persons who reported frequent lifetime cocaine use had a significantly higher likelihood of nonfatal MI than nonusers (odds ratio, 6.9; 95% confidence interval, 1.3 to 58) but not stroke. In this age group, the population-attributable risk percent of frequent cocaine for nonfatal MI was estimated as 25%.

CONCLUSION:

Regular cocaine use was associated with an increased likelihood of MI in younger patients. Approximately 1 of every 4 nonfatal MIs in persons aged 18 to 45 years was attributable to frequent cocaine use in this survey. Behavior modification by public awareness and education may reduce the cardiovascular morbidity associated with cocaine use.
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PMID:
11157713
[PubMed - indexed for MEDLINE]
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14. AJNR Am J Neuroradiol. 2000 Jun-Jul;21(6):1008-10.

Moyamoya-like vasculopathy from cocaine dependency.

Storen EC, Wijdicks EF, Crum BA, Schultz G.

Source

Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, MN 55905, USA.

Abstract

We herein describe two cases of moyamoya vasculopathy occurring in two men who used alkaloidal cocaine for years. One patient presented with aneurysmal subarachnoid hemorrhage and one with infarction in both lobes. Particularly impressive was a significant degree of collateral development with lenticulostriate networks.
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PMID:
10871003
[PubMed - indexed for MEDLINE]
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15. Chest. 2000 Jan;117(1):275-7.

Cocaine-induced bradyarrhythmia: an unsuspected cause of syncope.

Castro VJ, Nacht R.

Source

State University of New York Health Science Center at Brooklyn, Brooklyn, NY, USA.

Abstract

Cocaine use is associated with adverse events in nearly every organ system. Cardiovascular complications include hemorrhagic and ischemic stroke, aortic dissection, cardiomyopathy, accelerated coronary artery disease, myocardial infarction, and sudden cardiac death. Syncope may be the presenting symptom in these conditions. However, cocaine-induced bradyarrhythmias have been scarcely mentioned. As this case exemplifies, clinicians should be aware of this association when they evaluate syncope, especially in young patients.
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PMID:
10631230
[PubMed - indexed for MEDLINE]
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16. AJNR Am J Neuroradiol. 1999 Oct;20(9):1628-35.

The incidence of T2-weighted MR imaging signal abnormalities in the brain of cocaine-dependent patients is age-related and region-specific.

Bartzokis G, Goldstein IB, Hance DB, Beckson M, Shapiro D, Lu PH, Edwards N, Mintz J, Bridge P.

Source

Mental Health Service Line, Central Arkansas Veterans Healthcare System, Little Rock 72114, USA.

Abstract

BACKGROUND AND PURPOSE:

Cocaine and its metabolites can produce vasospasm, and cocaine-dependent patients are at increased risk for stroke. Based on previous case reports, we hypothesized that the incidence of hyperintense brain lesions observed on T2-weighted MR images would also be increased in asymptomatic cocaine-dependent individuals.

METHODS:

Sixty-two male "crack" (smoked) cocaine-dependent participants ranging in age from 25 to 66 years were compared with 116 normal male control participants ranging in age from 25 to 80 years. Those with histories of neurologic symptoms or illnesses were excluded. The severity of hyperintense lesions was rated on a 0- to 3-point scale, and ratings of 3 were used in the data analysis as an indicator of a probable pathologic process. Three regions were separately rated: the cerebral white matter, insular subcortex white matter, and subcortical gray matter (basal ganglia and thalamus region).

RESULTS:

Significantly increased risk of severe lesions was observed in the two white matter regions of the cocaine-dependent group (odds ratio of 16.7 and 20.3) but not in the subcortial gray matter region (odds ratio of 1.4). In the insula subcortex white matter, the risk of lesions increased with age in the cocaine-dependant sample, but remained essentially absent among normal controls through the age of 80 years. In the cerebral white matter, the relationship of age and risk of lesion among normal participants was similar in shape to that in cocaine-dependent participants, but equivalent risk was seen 20 years earlier among cocaine-dependent participants.

CONCLUSIONS:

Cocaine-dependent participants had a significantly increased age-related risk of white matter damage. The possible clinical implications of this damage are discussed.
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PMID:
10543632
[PubMed - indexed for MEDLINE]
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17. Stroke. 1991 Oct;22(10):1320-5.

Central nervous system infarction related to cocaine abuse.

Daras M, Tuchman AJ, Marks S.

Source

Department of Neurology, New York Medical College, Metropolitan Hospital, New York 10029.

Abstract

BACKGROUND:

Cocaine use in the United States has reached epidemic proportions, and increased availability of "crack" since 1983 has noticeably increased the incidence of neurovascular complications. In this report, we examine the relationship between cocaine use and ischemic infarct.

SUMMARY OF COMMENT:

This study reports 18 cases of ischemic cerebrovascular events, which occurred among 15 men and three women aged 21-47 years who were evaluated in a 2-year period. Clinical presentations include thirteen cases with hemispheric infarcts, two brain stem strokes, two anterior spinal artery infarcts, and one with both hemispheric and cerebellar infarcts. Nine patients smoked crack, four snorted cocaine, and three injected it intravenously. In two cases, the route of administration could not be determined. Two patients died, but the other survived with various degrees of neurological deficit.

CONCLUSIONS:

Traditional risk factors for strokes were identified in only six patients, suggesting that these factors are not necessary for the occurrence of a cocaine-related infarct. Multiple overlapping mechanisms may be responsible, including vasospasm, sudden onset of hypertension, myocardial infarction with cardiac arrhythmias, increased platelet aggregation, and vasculitis.
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PMID:
1926246
[PubMed - indexed for MEDLINE]
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18. Stroke. 1991 Sep;22(9):1203-5.

Recurrent embolic stroke and cocaine-related cardiomyopathy.

Sauer CM.

Source

Department of Neurology, University of Tennessee, College of Medicine, Memphis.

Abstract

Ischemic stroke temporally related to cocaine abuse has become increasingly common in young adults. Despite this relation, however, the pathogenesis of infarction in many of these patients remains obscure. I report the case of a 39-year-old man who developed occlusion of the frontopolar branches of the left middle cerebral artery 1 hour after intravenous cocaine use. Eleven days later he developed occlusion of the superior division of the right middle cerebral artery. In this case the mechanism of infarction was clearly cardiogenic embolization. Chest radiograph and echocardiogram revealed dilated cardiomyopathy with left ventricular thrombi. No cause other than cocaine abuse was found for his cardiomyopathy. This is the second reported case of cocaine-related cardiomyopathy presenting as embolic stroke and associated with intracavitary thrombus. Such an association may be more common than previously thought. Thorough cardiac evaluation in all patients with ischemic stroke related to cocaine abuse is appropriate.
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PMID:
1926265
[PubMed - indexed for MEDLINE]
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19. N Engl J Med. 1990 Sep 13;323(11):699-704.

Cerebrovascular complications of the use of the "crack" form of alkaloidal cocaine.

Levine SR, Brust JC, Futrell N, Ho KL, Blake D, Millikan CH, Brass LM, Fayad P, Schultz LR, Selwa JF, et al.

Source

Department of Neurology, Henry Ford Hospital and Health Science Center, Detroit, MI 48202-2689.

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 [2 hemorrhagic; 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 sever 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.
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PMID:
2388668
[PubMed - indexed for MEDLINE]
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20. Stroke. 1987 Jul-Aug;18(4):712-5.

Intracranial hemorrhage and cocaine use.

Wojak JC, Flamm ES.

Abstract

Cocaine use has increased rapidly over the past few years. This has led to an increase in the number and variety of cocaine-related conditions for which medical attention is sought. Among these have been several cases of intracranial hemorrhage. Four cases reported in the literature and 6 from our own institution are presented here. They represent different diagnoses including hemorrhage from aneurysms and arteriovenous malformations, hemorrhage into a tumor, and spontaneous hemorrhage with no underlying lesion with and without preexisting hypertension. Analysis of these cases suggests that the hypertension induced by cocaine secondary to sympathetic stimulation may be the common factor. Cocaine may also cause arterial spasm. Although the pathophysiology has not been entirely resolved, the clinical significance of this association is clear. Intracranial hemorrhage should be considered in the differential diagnosis whenever a patient presents with an acute alteration in neurologic examination associated with cocaine use.
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PMID:
3603597
[PubMed - indexed for MEDLINE]
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21. J Neurol Neurosurg Psychiatry. 1976 Feb;39(2):194-9.

Stroke associated with addiction to heroin.

Brust JC, Richter RW.

Abstract

During a five year period at the Harlem Hospital Center nine heroin addicts were seen with strokes. Four occurred after loss of consciousness following intravenous heroin. Two occurred in patients using heroin at the time, but were not related to overdose or to a particular recent injection. The youth of these patients and lack of other predisposing factors suggests that heroin played a role in their strokes. In the other three patients, the relationships of stroke to heroin is less persuasive. There are several possible mechanisms by which heroin abuse could lead to stroke.
PMCID: PMC492246
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PMID:
1262894
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