Scielo RSS <![CDATA[Salud mental]]> http://www.scielo.org.mx/rss.php?pid=0185-332520080004&lang=es vol. 31 num. 4 lang. es <![CDATA[SciELO Logo]]> http://www.scielo.org.mx/img/en/fbpelogp.gif http://www.scielo.org.mx <![CDATA[<b>La investigación biomédica en el Instituto Nacional de Psiquiatría Ramón de la Fuente, a 30 años de la aparición de <i>SALUD MENTAL</i></b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400001&lng=es&nrm=iso&tlng=es <![CDATA[<b>La otra migración. Historias de discriminación de personas que vivieron con VIH en México</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400002&lng=es&nrm=iso&tlng=es Mexican migration to the United States has been attributed to the poverty and economic polarization in Mexico. Although the dismantling of the peasant economy persists as a factor in demographic displacement, there have been recent changes in the causes that provoke the migration of Mexicans. Family violence, for example, appears as an important motivator in pushing women into the migratory flow, especially in rural areas of the country where women's sexual and reproductive rights appear to be less respected. Homophobia is another point of reference which, along with hate crimes, generates a new category of migration to the United States. Although violence is beginning to be recognized and viewed sociologically as a factor in migratory displacement, it is a phenomenon that has been little explored in Mexico until now. This article proposes to analyze sexual violence and discrimination as motivators of an emerging migratory phenomenon among transgender and transsexual groups within the Mexican population. The article is based on a qualitative study which explored the universes of sense and meaning through the stories of four Mexican women, three transgender and one transsexual, infected with HIV-AIDS in Mexico and who are currently seeking political asylum in San Diego, California. The fieldwork was done between August and September 2003 in San Diego County. Interviews and ethnographic observations were carried out in three geographic regions in the city where neighborhoods of transgender and transsexual migrants of Mexican origin were detected, as well as Non-Governmental Organizations (NGOs) that provide medical and psychological care to undocumented migrants of Latin American origin who live with HIV/AIDS: Northern Region: Carlsbad and Rancho Bernardo; Central Region: North Hill Park and Balboa Park; Southern Region: San Ysidro and Imperial Beach. The article provides anthropological data regarding the contexts, practices and magnitude of rejection and violence that the subjects suffered in Mexico. Four settings are emphasized: family life, interaction in the streets, the relationship with police and the relationship with health services related to caring for HIV/AIDS. To support the analysis it was considered advisable to resort, on the one hand, to phenomenology as a methodological approach to daily life and, on the other hand, to semiotics, where culture is understood as the expression of symbolic forms and objectivizations of sense and meaning that exist in the context of asymmetrical social relationships. This theoretical framework allowed us to postulate that sexual violence is a structural process based on asymmetrical power relationships and that it implies social norms and ideologies of male hegemony that contribute to the social acceptance of violent practices against transgender and transsexual men, which can make them go unnoticed in the community. For the interviewees, migration became a resort for asserting their right to health care, and even a means to preserve their lives. In Mexico, their presence in public places would frequently provoke attacks, scorn and mockery, which could lead to physical and emotional wounds. Civil society is not the only source of violence against transsexual and transgender individuals. Some police organizations systematically persecute them and submit them to violence. The harassment of homosexuals is routine practice among police officers. Their physical appearance is interpreted as a moral misdemeanor. Under this argument, they can become the victims of a complex range of abuses and humiliations that include blackmail or extortion and can lead to physical assault and sexual violence. This last type of aggression is one of the most dangerous because it implies a homosexual conduct on the part of the aggressor. Because there is a risk that his victim might press charges, the violence exercised against the transgender individual by the aggressor may be aggravated, which initiates a cycle of territorial mobility linked to exile because of the fear of being killed. Violence against transsexuals is reinforced by Mexican laws and bureaucratic procedures, which only recognize two genders and thus make it more complicated for transsexuals to prove their legal right to initiate proceedings or a lawsuit. These legal-bureaucratic loopholes help make the aggressor's impunity acceptable and his violations socially invisible. The stories make it possible to understand that in Mexico transphobia is a specific form of sexual violence which, linked to the social construction of male dominance, exists out of social fear of homosexuality as the foundation that legitimizes discrimination, hate, persecution and aggression against transgender and transsexual individuals. One aspect that seems to intensify these forms of violence is the appearance of sexually transmitted viral infections. In fact, the history of infectious diseases shows that homosexuals, sexual workers and migrants appear over and over again in the collective imagination as those responsible for the origin of epidemics. In today's epidemiological context, transgender is seen as a scapegoat for HIV/ AIDS. In Mexico, this situation appears to reinforce the preconceptions of social hatred against transgender persons who are HIV positive, who may end up living with the social stigma of those who believe that the infection is fitting punishment. The evidence suggests that, when transgender individuals are HIV carriers, discrimination against them is worse. The prejudice of medical personnel and the financial inability of health institutions to treat HIV/AIDS lead to precarious care and, occasionally, denial of access to antiretroviral medications. Ethnography suggests that violence against transsexuals is not eliminated when they immigrate to the United States. They experience less aggression than in Mexico, but in the United States they suffer racial and job discrimination. The benefit resides in that, despite their undocumented status, they have free access to antiretroviral drugs and to psychological care offered by the NGOs in San Diego that assist persons infected with HIV/AIDS. The discrimination and sexual violence described by those interviewed amount to a triple stigmatization (because they are itinerant populations, because they are transgender and because they live with HIV). This is a system of stigmatization that not only affects their quality of life by excluding them from jobs and the legal system, but also because it keeps them from being recognized as subjects with rights to health care, especially with regard to access to antiretroviral drugs and medical care related to control of HIV/AIDS, decisive factors which trigger the decision to migrate. This paper suggests the development of a model aimed at making medical practitioners and, in general, health systems personnel more aware of the diversity of sexual practices and identities and emphasizes the right to sexual and mental health care for individuals who live with HIV, regardless of their sexual preference or gender. It is fundamental to develop policies that will prevent the stigmatization and discrimination of persons with HIV and that will recognize the right to health care among populations that have been stigmatized historically.<hr/>La migración mexicana a Estados Unidos se ha interpretado como un proceso demográfico que existe en respuesta al empobrecimiento y a la polarización económica en México. Aunque la desarticulación económica y el abandono de las regiones rurales de México persisten como factores de expulsión de población, la migración de mexicanos muestra cambios recientes en las causas que la originan. La violencia familiar, por ejemplo, aparece como un detonante importante de la incorporación de la mujer en los flujos migratorios, particularmente es el caso de zonas rurales del país. La homofobia es otro referente que, relacionado a los crímenes de odio, parece generar un nuevo orden de migración hacia Estados Unidos. No obstante que la violencia empieza a ser reconocida y vista sociológicamente como un factor de expulsión migratoria, en México es un fenómeno que hasta ahora se ha explorado poco. En este trabajo se analizan la violencia sexual y la discriminación como detonantes de un fenómeno migratorio emergente entre grupos de población homosexual. Se trata de un estudio cualitativo de tipo fenomenológico con el que se exploraron los universos de sentido y significado por medio de las historias de vida de migrantes transgénero y transexuales que viven con VIH en San Diego. El trabajo de campo se realizó en agosto de 2003 en condados de San Diego, California, en Estados Unidos. Se realizaron entrevistas y observaciones etnográficas en tres regiones geográficas de la ciudad donde se detectó la presencia de vecindarios de migrantes transgénero y transexuales de origen latinoamericano. En este artículo se describen precisamente las historias de personas transgénero y transexuales que se infectaron de VIH-sida en México. Para estas personas, la migración se convirtió en un recurso para atender su derecho a la salud e incluso para conservar la vida. El objetivo de este artículo es dar cuenta de las formas de agresión física y de discriminación que llevaron a los entrevistados a solicitar asilo político en San Diego, California. Las narraciones permiten comprender que en México la transfobia es una forma de violencia sexual que, ligada a la construcción social de la masculinidad dominante, existe a partir del miedo social a la homosexualidad como el basamento que legitima la discriminación, la persecución y la agresión de personas transgénero y transexuales. Un aspecto que parece recrudecer estas formas de violencia es la aparición de infecciones sexualmente transmisibles de tipo viral. De hecho, la historia de las enfermedades infecciosas muestra que homosexuales, trabajadoras sexuales y migrantes son figuras que aparecen de manera recurrente en el imaginario colectivo como responsables del origen de las epidemias. En el contexto global actual destaca la construcción del transgénero como víctima propiciatoria del VIH/sida. En México, esta coyuntura parece reforzar los esquemas de odio social en contra de las personas homosexuales que son VIH positivas, quienes pueden llegar a vivir con el estigma social de quien cree que la infección es un castigo meritorio. La discriminación y la violencia sexual que describen las informantes tiene que ver con la triple estigmatización (por ser poblaciones móviles, por ser transgénero y además por vivir con VIH). Se trata de un sistema de estigmatización que no sólo afecta la calidad de vida al excluirles laboral y jurídicamente, sino que impide reconocerles como sujetos de derecho a la salud, especialmente en materia de acceso a medicamentos antirretrovirales y de atención médica relativa al control del VIH/sida. Es necesario desarrollar un modelo de sensibilización dirigido a personal médico y, en general, de los sistemas de salud sobre la diversidad de prácticas e identidades sexuales y hacer énfasis en los derechos a la salud sexual y mental de las personas que viven con VIH, sin importar su preferencia sexual y de género. <![CDATA[<b>Estudio de casos y controles en un grupo de mujeres embarazadas con experiencias adversas en la infancia y/o adolescencia e infecciones de transmisión sexual</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400003&lng=es&nrm=iso&tlng=es Introduction Psychic traumas, also called adverse experiences, are events from the subject's life characterized by its intensity, the subject's inability to respond to them properly and the pathogenic lasting effects they cause in the psychic organization. The violence effects against women and girls are usually devastating for their reproductive health and other aspects of their physical and mental well-being. Besides injuries, violence causes an increase in the long-term risk of women developing other health problems. Women with a history of psychic mistreat or sexual abuse face also a bigger risk of non-expected or involuntary pregnancies, sexual transmitted infections and adverse results from pregnancy. High rates of childhood abuse were found: 42.2% had suffered physical mistreat, 21.4% had been insulted, 16.5% was victim of humiliation and 7.6% had been a victim of sexual abuse before fifteen years of age. The main aggressors were male relatives, the stepfather or the father. A study done in the United States found that women exposed to this form of violence suffered STI in adult age in a bigger proportion (10.7%) than the ones that were never exposed (5.7%). An investigation was made in the National Perinatolgy Institute called «STD/HIV-AIDS and Personality Disorders (PD) in pregnant women and their couples. Detection and prevention from high risk practices» with the objective -among others- to resolve the existing association between adverse experiences in childhood and the presence of sexually transmitted infections in gestation. Material and method The investigation design was of cases and controls; the characteristics of the study in relation to temporality was prospective with respect to the presence or absence of the pathogenic agent in gestation and retrospective (investigating adverse experiences in childhood), analytical referring to the analysis type and transverse with respect to the capture of the sample. The evaluation of the STIs was made through the Laboratory of the Sexually Transmitted Infections Clinic of the INPer and from the pertinent clinic exams. The diagnostic evaluation was made on the basis of the structured clinic interviews for the diagnostic psychiatric evaluation of I and II axes of DSM-IV. To investigate adverse childhood experiences, a psychodynamic interview was made and answers were transcribed then to the questionnaire made by Whitfields, Dube, Felitti and Anda, who developed the instrument Adverse Experiences in Childhood and/or Adolescence (ACE) with the aim to measure the amplitude of the exposition to emotional, physical and sexual abuse, as well as family dysfunction in these stages of life. It includes seven categories of adverse experiences, three relative to active abuse and five to passive abuse: 1. psychological abuse; 2. physical abuse; 3. sexual abuse; 4. conjugal violence against the mother; 5. living with parent or adults with alcohol problems and/or substance abusers; 6. living with parents or adults with mental disorders or suicidal; 7. living with parents that had been in jail. Results One hundred seventy-eight pregnant women were divided in two groups, the first one with 89 participants, in which a virus that caused the STI was identified, and the second group was the control group with also 89 pregnant women without STI. Significant differences were obtained in the socioeconomic level. There was also a significant association between fathers of the women with STI that had some legal problem and had being sent to jail for a period of time (RM 3.311); they also show small alcoholic problems (RM 2.073). There was a significant association with the different types of passive abuse (carelessness, negligence and indifference) physical, emotional and sexual, emphasizing that the relation between these categories and having an STI by a virus is highly significant; this is, being exposed in childhood to adverse events, more probability to get a viral STI in adulthood. The cases group accumulated three or more in bigger proportion (20.2%) than the control group (9%). The STI pregnant group presented a bigger number of traumatic events (69.9%) in comparison to the group with no STI that was 48.3%. It is appraised the bigger prevalence of mental disorders in the STI pregnant group, having a disorder increased the potential risk of infection by 2.45 times (C:I to 95% that oscillates between 1.303 and 4.61). Conclusions The STI viral group and the control group are different concerning socioeconomic level and schooling, finding in the STI group a bigger proportion of women whose monthly family income is lower, the poverty as a risk factor and/or social vulnerability for the HIV infection, the interaction between living in poverty conditions and the difficulty to access and to stay in the national educative system are closely related. In addition, this case group was integrated in a bigger proportion with pregnant who were not united in the study period. It is important to mention that half of the pregnant that formed the HIV/ AIDS group suffered the pain of seeing their couple die. From the adverse experiences in childhood and/or adolescence that could have been in the start or been a beginning factor for getting afterwards a viral STI in adulthood, the significant ones were having lived with a alcohol abuser adult, thus being victim of carelessness, negligence or indifference, same as being hit, pushed, pushed or hit so hard to leave marks, humiliations, coarses, insults, feelings of being less and victim of being touched or having a sexual experience. These traumatic events happened simultaneously, mainly in the cases group where 40 pregnant declared being exposed to two or more categories in contrast with 22 of the control group. Alcohol abuse is a generalized health problem and common in all societies; pregnant women with STI were in bigger proportion more exposed to familiar alcohol than the control group and approximately half of them were at the same time victims of some forms of abuse or violence by their fathers or stepfathers. Studies made in 21 countries show that between 7% and the 36% of the women had accepted being victims of sexual aggressions during their childhood and, according to most of these studies, the rate of abuses suffered by girls is 1.5 to 3 times bigger than men. The same report makes evident the fact that between 133 and 275 millions of children from all over the world are witnesses of domestic violence each year; this is, witness violent scenes at their home, generally through fights between their parents or between their mother and couple, which can also seriously affect their well-being, development and their social interaction in childhood and adult age. It has also been found that suffering an active abuse in childhood is a risk factor for structuring a borderline personality disorder.<hr/>Resumen Introducción Los traumas psíquicos, también denominados experiencias adversas, son acontecimientos de la vida del sujeto caracterizados por su intensidad, la incapacidad del sujeto para responder a ellos adecuadamente y los efectos patógenos duraderos que provocan en la organización psíquica. Los efectos de la violencia contra las mujeres y las niñas suelen ser devastadores para la salud reproductiva de la mujer y otros aspectos de su bienestar físico y mental. Además de causar lesiones, la violencia lleva a que aumente el riesgo a largo plazo de que las mujeres desarrollen otros problemas de salud. Las mujeres con una historia de maltrato físico o abuso sexual también enfrentan un riesgo mayor de embarazos no previstos o involuntarios, infecciones de transmisión sexual (ITS) y resultados adversos del embarazo. En el Instituto Nacional de Perinatología se realizó una investigación titulada «ETS/VIH-SIDA y trastornos de la personalidad en mujeres embarazadas y sus parejas. Detección y prevención de prácticas de alto riesgo» con el objetivo -entre otros- de determinar la asociación existente entre experiencias adversas en la infancia y la presencia de infecciones de transmisión sexual en la gestación. Material y método El diseño de la investigación fue de casos y controles; el estudio fue prospectivo respecto de la presencia o ausencia del agente patógeno en la gestación y retrospectivo (indagación de experiencias adversas en la infancia). La evaluación de las ITS se efectuó por medio del laboratorio; la evaluación diagnóstica se efectuó con base en las Entrevistas Clínicas Estructuradas para la evaluación diagnóstica psiquiátrica de los Ejes I y II del DSM-IV. Se aplicó el instrumento Experiencias Adversas en la Infancia y/o Adolescencia (ACE, por sus siglas en inglés), con el fin de medir la amplitud de la exposición al abuso emocional, físico y sexual, así como la disfunción familiar en estas etapas de la vida. El instrumento comprende siete categorías: 1. abuso psicológico; 2. abuso físico; 3. abuso sexual; 4. violencia conyugal contra la madre; 5. vivir con padres o adultos con problemas de alcoholismo y/o que eran abusadores de sustancias; 6. vivir con padres o adultos con trastornos mentales o suicidas; 7. vivir con padres que fueron encarcelados. Resultado Se estudiaron dos grupos, el primero de casos integrado con 89 embarazadas con ITS viral y el segundo fue el grupo control integrado también con 89 gestantes, sin ITS. Se obtuvieron diferencias significativas en el nivel socioeconómico. Así mismo hubo una asociación significativa entre los padres de las mujeres con ITS que tuvieron algún problema con la ley por lo que habían sido encarcelados por un determinado periodo de tiempo (la razón de momios fue 3.311); y los que manifestaron leves problemas de alcoholismo (RM 2.073). Hubo una asociación significativa en: abuso pasivo, físico, emocional y sexual, donde destaca que la relación entre estas categorías y padecer una ITS por virus es altamente significativa. El grupo de las gestantes con ITS presentó un mayor número de problemas traumáticos (69.9%) en comparación con el grupo sin ITS que fue de 48.3%. Conclusiones De las experiencias adversas en la infancia y/o adolescencia, que pudieron estar en el origen o haber sido un factor iniciador para adquirir posteriormente una ITS de origen viral en la edad adulta, fueron significativas haber convivido con un adulto cercano con problema de abuso del alcohol y haber sido víctima de descuido, abuso físico, emocional o sexual. <![CDATA[<b>Prevalencia del consumo riesgoso y dañino de alcohol y factores de riesgo en estudiantes universitarios de primer ingreso</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400004&lng=es&nrm=iso&tlng=es Background In Mexico, alcohol is the most widely used substance among young adults. Alcohol consumption in this age group contributes importantly to the most frequent causes of mortality and morbidity (e.g., accidents, violence, homicides, suicide and risky behaviors). Around the world, college or university attendance has emerged in the literature as a risk factor for drinking problems among young adults. In Mexico, data from the most recent National Survey on Addictions showed that lifetime and current drinking is experienced by more than half of the Mexicans attending college education. Despite this, in our country there is a paucity of epidemiological studies examining drinking behavior and correlates among those attending college. Findings in non-representative samples of students attending public and private universities in Mexico City suggest that, during the last two decades, there has been an increase in the frequency of lifetime and current drinking in this population. Additionally, these studies have shown that, in comparison to young adults of the same age in the general population, university students may experience a greater prevalence of lifetime and current alcohol drinking. Regarding the frequency of unhealthy drinking among Mexican college students, to our knowledge there are no prevalence estimates of hazardous or harmful drinking published. However, observations in non-random samples of university students in Mexico City suggested that at least one in three men and one in five women incurred in unhealthy drinking (e.g., ≥ 5 drinks per occasion or drinking to intoxication) at least once during the last month. Hazardous and harmful drinking is respectively defined by a pattern of alcohol consumption conferring a greater risk for health problems or that is frankly conducive to medical or psychological complications (e.g., accidents, victimization, violence, alcohol dependence, liver cirrhosis and/or other medical complications). The Alcohol Use Disorders Identification Test (AUDIT), developed by the World Health Organization, is currently the only instrument specifically designed to identify hazardous and harmful drinking. Although the AUDIT was initially validated among older adult patients in primary care settings, this instrument has consistently shown to be valid and reliable in detecting alcohol problems in different populations such as the college students in many countries around the world. Given the public health implications of estimating the frequency of hazardous and harmful drinking among college students in Mexico, and given the importance of elucidating the variables influencing this problem, we decided to conduct the present study. To our knowledge, this is the first report published in the international literature on the prevalence of hazardous and harmful drinking among college students in a Latin American country. Objective In the analysis described here, derived from the project entitled Early Identification and Treatment of Problem Drinkers at the National Autonomous University of Mexico (UNAM), our aim was to examine the frequency and risk factors for hazardous and harmful drinking among Mexican university students. More specifically, our objectives were: 1. To determine the past-year prevalence of hazardous and harmful drinking among UNAM college freshmen; and 2. To examine in this population the effects of demographic and family variables on the likelihood of hazardous and harmful drinking. Subjects and methods This study was a cross-sectional survey that was conducted at the beginning of the school year during the registration period between September 1st and September 30th, 2005. In 2005, a total of 34 000 students were accepted to initiate college at the nine UNAM college campuses located in the Mexico City metropolitan area. Of these, 24 921 (73.3%) students (age=18.7±4.3 years; 55.7% women) consented in answering the survey and provided complete data. Consequently, 9 079 students (26.7%) were excluded from the analysis due to lack of consent, incomplete data or due to their absence at the time of registration. We used the Alcohol Use Disorders Identification Test (AUDIT) to examine past-year prevalence of hazardous and harmful drinking. This self-report instrument includes 10 items that examine frequency and intensity of drinking (items 1-3), presence of alcohol dependence symptoms (items 4-6) and negative consequences of drinking (items 7-10), yielding a maximum possible score of 40 points. Among adult patients in primary care settings, it has been accepted that an AUDIT score of 0-7 points reflects safe levels of alcohol consumption, whereas a score of 8 points or greater indicates the presence of hazardous and harmful drinking. It has been described, however, that among college students, an AUDIT score of 6 points or greater reliably identifies those students experiencing this problem. In the analysis presented here, we separately examined and reported the prevalence estimates and correlates of hazardous and harmful drinking using both AUDIT cut-off scores (≥ 6 and ≥ 8). The AUDIT was administered at the same time as a wellness screening survey that the UNAM Medical Services routinely administer to all registering freshmen at the beginning of the school year. Questions in the wellness survey pertained students' medical and dental health, family medical history, immunizations, use of tobacco and other drugs. In addition, demographic and socioeconomic information was obtained from a questionnaire also routinely administered by the UNAM registrar's office. This questionnaire included 37 items inquiring about gender, age, employment and marital status, monthly family income, parental education, place and type of residency, persons with whom the student resided, and questions on previous academic performance.<hr/>Antecedentes En México, el alcohol es la sustancia potencialmente adictiva que se utiliza con mayor frecuencia por los adultos jóvenes. Información proveniente de la Encuesta Nacional de Adicciones más reciente muestra que más de 50% de los jóvenes entre los 18-29 años ha consumido bebidas alcohólicas al menos una vez durante el último mes. En la Ciudad de México se ha encontrado que más de la mitad de las mujeres y cerca de dos terceras partes de los hombres entre 18-29 años de edad consume regularmente bebidas alcohólicas. Durante los últimos años, el consumo de bebidas alcohólicas se ha venido incrementando importantemente entre los jóvenes mexicanos de ambos sexos en edad de recibir una educación superior. A nivel internacional, la bibliografía sugiere que la población estudiantil de los centros de educación superior es un grupo de mayor riesgo para el desarrollo de problemas por consumo de alcohol. En México, aunque se desconoce si los estudiantes de educación superior son un grupo de mayor riesgo para estos abusos, algunas encuestas y reportes sugieren que los problemas por consumo de alcohol tienen una importancia creciente. En cuanto al consumo de alcohol que excede los niveles seguros para la salud (≥2 bebidas estándar al día en las mujeres o ≥3 bebidas estándar al día en los hombres), el Observatorio Mexicano del Alcohol y Drogas describió que en el año 2002 el consumo de cinco o más copas por ocasión de consumo afecta a tres de cinco hombres y a una de cinco mujeres. Aunque problemas metodológicos y sesgos de selección potenciales en estas encuestas dificultan su interpretación, sus resultados sugieren que el consumo de alcohol, particularmente el consumo riesgoso y potencialmente dañino, es común entre los estudiantes universitarios de la Ciudad de México. El consumo riesgoso y dañino de alcohol (CRDA) se sitúa en un continuum de severidad y se define como un patrón de consumo de bebidas embriagantes que colocan al sujeto en riesgo de desarrollar problemas de salud y/o que desemboca en francas complicaciones físicas y/o psicológicas (accidentes, victimización, violencia, dependencia al alcohol, cirrosis hepática, etc.). De acuerdo a los reportes de la bibliografía internacional, este es el primer estudio publicado sobre la prevalencia de consumo peligroso y dañino de alcohol en estudiantes universitarios en América Latina. Objetivo En el trabajo que se presenta aquí, que forma parte del proyecto para la Identificación Temprana y Tratamiento Oportuno de bebedores con Consumo Excesivo de Alcohol en Estudiantes Universitarios de la UNAM, nos propusimos evaluar la prevalencia del CRDA durante el último año y examinar los factores de riesgo y protección respectivos en estudiantes de primer ingreso a la licenciatura de la Universidad Nacional Autónoma de México. De manera especifica, nos propusimos: 1) estimar la prevalencia del CRDA durante el último año en los estudiantes de primer ingreso a la licenciatura de la UNAM, y 2) evaluar en esta población la influencia de las variables sociodemográficas y familiares en el riesgo para el CRDA. Material y métodos Se trató de un estudio transversal en el que se estudiaron 24921 estudiantes del primer año de la licenciatura de la UNAM (edad=18.7±4.3 años; 55% mujeres). Para detectar aquellos estudiantes que en el último año incurrieron en el CRDA, se utilizó el instrumento de tamizaje Alcohol Use Disorder Identification Test (AUDIT). Se utilizó la regresión logística multinomial para examinar los efectos de las variables demográficas y sociofamiliares, así como para calcular Odds Ratios (OR) y sus respectivos intervalos de confianza al 95%. Este instrumento consiste de 10 preguntas que exploran la frecuencia e intensidad del consumo de bebidas alcohólicas. Con el objetivo de poder comparar nuestros hallazgos con los de otros investigadores, se examinaron y se reportan separadamente las prevalencias del CRDA con base en puntos de corte de 8 y de 6 en el AUDIT. Para el reporte de datos demográficos y puntajes del AUDIT, se utilizaron porcentajes, promedios y desviaciones estándar. Se emplearon las pruebas de contraste de medias (análisis de varianza) y de proporciones (χ2) dependiendo de la naturaleza de cada variable. Se calcularon las prevalencias del CRDA con sus respectivos intervalos de confianza al 95%. Resultados Usando un puntaje de corte en el AUDIT de ocho y de seis puntos, la prevalencia del CRDA durante el último año fue respectivamente de 11.1% y de 18.4%. Esta fue mayor en los hombres (AUDIT≥8: 17.3%; AUDIT≥6: 27.4%) que en las mujeres (AUDIT≥8: 6.2%; AUDIT≥6: 11.3%). Además del sexo masculino, aquellos estudiantes que trabajaban y que reportaron un mayor ingreso familiar mensual, tuvieron un mayor riesgo de experimentar el CRDA. En las mujeres, pero no en los hombres, un mayor nivel educativo tanto en el padre como en la madre también se relacionó con un incremento en el CRDA. Contrariamente, una mayor edad y el ser casado se asoció con una reducción en el riesgo del CRDA. <![CDATA[<b>Trastorno obsesivo-compulsivo en niños y adolescentes: Una actualización. </b><b>Segunda parte</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400005&lng=es&nrm=iso&tlng=es During the last years obsessive-compulsive disorder (OCD) has been reported with increased prevalence in pediatric population; this is due to the development of more specific assessment methods. This evolution in the evaluation tools has given rise to the possibility of characterizing OCD presentation in children and adolescents. In childhood, OCD is a chronic and distressing disorder that can lead to severe impairments in social, academic and family functioning. Current diagnosis criteria for pediatric OCD are the same than those used in adults. During all life span, obsessive and compulsive symptoms are necessary to establish the presence of the disorder. There are several different clinical manifestations among age groups, different evolution among children, adolescents and adults; all these represent a diagnostic and therapeutic challenge for the clinician. Several classifications incorporate pediatric OCD, especially those related to the familiar presentation form and patterns of comorbidity, mainly with tics disorders. At least 50% of children and adolescents with Gilles de la Tourette syndrome develop obsessive-compulsive symptoms or OCD in adulthood and almost a half of early-onset OCD subjects have a tics history. These findings support the notion that tics disorders are the comorbidity more closely related with early-onset OCD, giving elements to consider this association as a specific pediatric OCD subtype. In this age group population, comorbidity has been reported as high as in adulthood; some diagnoses are especially prevalent during childhood and others during adolescence. On the whole, anxiety disorders are frequent with OCD, generalized anxiety disorder, panic attack, social phobia and anxiety separation disorder. Comorbidity related with affective disorders is high too. The OCD association with major depressive disorder (MDD) in childhood is low but increases in adolescence; MDD reaches similar adult comorbidity rates in adolescence. Higher comorbidity prevalence of MDD has been found more related to the duration of OCD-illness than early-onset. Bipolar disorder (BD) is another frequent comorbid entity with great clinical relevance. When BD is the main diagnosis, comorbidity with OCD shows a prevalence of 16%; when OCD is the main diagnosis, comorbidity with BD shows a prevalence of 44%, showing an unidirectional relation. Some studies have shown even higher comorbidity prevalence of BD when considering bipolar spectra dimension as hypomania and cyclothymic disorder (30% and 50%, respectively) in OCD samples. Adults with OCD and BD comorbidity have more frequent episodic form, a greater number of concurrent mayor depressive episodes and a higher rate of religious or sexual obsessions. Adults with OCD without BD comorbidity show more rituals and compulsions. A recent study in pediatric population with BD and OCD found that BD type II was the must common related diagnosis, when age was considered, subjects with bipolar disorder resulted to have an earlier onset of OCD. Other comorbid diagnoses frequently reported in this early-onset OCD population are externalizing disorders as attention deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD). Children and adolescents with OCD have high rates of comorbid ADHD; this co-occurrence seems to be bidirectional. There is a consistent preponderance of males in most epidemiological studies. The onset of ADHD preceded the onset of OCD and the onset of OCD was earlier when ADHD was comorbid. Children with OCD plus ADHD compared with peers with OCD without ADHD show higher attentional and social problems, as well as aggressive high scores. ADHD is a risk factor for ODD. A valid and reliable clinical interview is needed to establish differential diagnosis among OCD and other compulsive behaviors and intrusive thoughts present in disorders like anorexia nervosa, body dysmorphic disorder, hypochondrias, tics disorders and impulse control disorders. All these categories have been considered as part of the obsessive-compulsive disorders spectrum. It is important to establish the difference between obsessions with poor insight common in early-onset OCD and overvalued ideas or delusions. Pervasive disorders as autism and Asperger syndrome frequently show stereotyped behaviors which may be considered as obsessive-compulsive symptoms. The diagnostic evaluation of children and adolescents with OCD includes a careful assessment and review of current and past obsessive-compulsive symptoms and comorbid conditions. This evaluation requires interviewing both child/adolescent and parents and usually requires more than one session. For children who do not regard their symptoms as excessive, information from parents, and if possible from teachers, is essential to identify the range of symptoms, severity and context. Many children and adolescents feel confused and embarrassed with their symptoms. It is important to dedicate time to build a true clinical alliance to elicit the story of their symptoms, as well as the impact on a child's thoughts and feelings. There are several useful instruments to establish OCD diagnosis and severity in children and adolescents. Self-report questionnaires have been used to identify the presence and severity of OCD symptoms. The most used self-rated measures for pediatric OCD are the 44-item Leyton Obsession Inventory-Child version (LOI-CV) and its shorter version, the 20-item LOI-CV Survey Form, and the Maudsley Obsession-Compulsion Inventory (MOCI). Clinician-administered interviews may be a more reliable method to identify obsessive-compulsive disorders in youth. The Childs Yale-Brown Obsessive-Compulsive Scale (CY-BOCS) is a commonly used Clinician-Rated measure of OCD symptoms derived from the Adult Yale-Brown Obsessive-Compulsive Scale. CY-BOCS Spanish version was translated in México and as the original version it must be applied to parents and children/adolescents separately; the clinician establishes then the best clinical information with all the data. The initial CY-BOCS section consists of a symptom checklist covering a comprehensive array of obsessions and compulsions. The severity score is derived from the second section of the measure in which global rating of time spent, interference, distress, resistance and control associated with obsessions and compulsions are generated. Separate scores are obtained for obsessions and compulsions, which, when combined, yield a total severity score of a maximum 40 points. Scores greater than or equal to 16 indicate clinically significant OCD in children and adolescents. The knowledge we now have about pediatric OCD pharmacotherapy is better. Several studies have demonstrated the efficacy of clorimipramine. This was the first agent approved for use in pediatric populations with OCD. Subsequent multisite randomized, placebo-controlled trials of selective reuptake inhibitors (SSRIs) have also demonstrated significant efficacy in pediatric population. Almost all meta-analysis with SSRIs studies in children and adolescents with OCD have proved their efficacy. The most common adverse effects of SSRIs are nausea, insomnia, activation and headache. These effects are transient and most children tolerate them. The availability and effectiveness of SSRI have changed dramatically the OCD treatment, and neurobiological and neuroimaging advances have supported their use. Many children and adolescents with OCD need multiple treatments including cognitive behavior therapy (CBT), pharmacologic treatment, parental, family and teachers training. These interventions need to be applied by experts in order to be effective. CBT is a well-documented and effective intervention for adults with OCD. The potential usefulness of CBT for pediatric OCD has been valued and the results report that combined CBT and pharmacotherapy have proved high and sustained response in children and adolescents with OCD.<hr/>El trastorno obsesivo-compulsivo (TOC) se ha reportado en los últimos tiempos con mayor prevalencia en la edad pediátrica que lo reportado anteriormente gracias a una mejor caracterización de su presentación en niños y adolescentes y al desarrollo de mejores métodos de evaluación. Por sus características en la infancia el TOC ha dado pauta a diversas clasificaciones, una de estas formas de clasificación está condicionada por la coexistencia o comorbilidad con otros trastornos. Los tics o Trastorno de Gilles de la Tourette están fuertemente relacionados con un inicio temprano y con agregación familiar; la mitad de los niños y adolescentes con síndrome de Gilles de la Tourette desarrollan TOC. El 60% de los niños y los adolescentes que acuden a buscar tratamiento por TOC han tenido historia de trastornos por tics a lo largo de la vida. La comorbilidad del TOC con otros problemas ansiosos durante la infancia y la adolescencia es alta, en especial con el trastorno de ansiedad por separación, la fobia social, el trastorno de ansiedad generalizada y las fobias específicas. El trastorno depresivo mayor (TDM), es frecuentemente comórbido, más en los adolescentes que en los niños, el TDM comórbido se ha vinculado más con la duración del TOC que con la edad de inicio temprano. Con respecto al trastorno bipolar (TB), los reportes también muestran importante relación con el TOC. Las investigaciones de comorbilidad han estudiado el impacto del TB sobre el curso del TOC y encontraron mayor frecuencia de: curso episódico, episodios depresivos, deterioro funcional, hospitalizaciones y uso de polifarmacia. Otras investigaciones sobre esta comorbilidad TB/TOC vs. TOC han reportado mayor frecuencia del diagnóstico de TB tipo II y mayor asociación con inicio temprano del TOC. También se ha reportado frecuentemente la comorbilidad con los trastornos externalizados y particularmente con el trastorno por déficit de atención e hiperactividad (TDAH), que se ha asociado con un inicio más temprano del TOC, disfunción social y académica. Este patrón comórbido TOC/TDAH está vinculado a mayores problemas de inatención y conductas agresivas y se presenta más frecuentemente en hombres. El TDAH es un factor de riesgo para presentar trastorno negativista y desafiante o trastorno disocial en la adolescencia. Otras comorbilidades importantes a considerar son los trastornos del espectro obsesivo-compulsivo como los trastornos del control de los impulsos, trastorno dismórfico corporal y de la conducta alimentaria y trastorno sexual compulsivo. La comorbilidad con trastornos psicóticos como la esquizofrenia debe ser tomada en cuenta. En la evaluación de niños y adolescentes con TOC se requiere una investigación exhaustiva sobre los síntomas obsesivos-compulsivos actuales y pasados, así como su comorbilidad e historia familiar. Las entrevistas con los niños requieren de la participación de los padres y profesores. Muchos niños y adolescentes se sienten avergonzados por sus síntomas por lo que es importante dar tiempo necesario para lograr la confianza del chico para hablar de sus síntomas. Existen diversos instrumentos útiles para establecer la severidad del TOC en niños y adolescentes. Entre los cuestionarios auto-aplicables se encuentra el Inventario de Obsesiones de Leyton (LOI) y el inventario de obsesiones y compulsiones de Maudsley (MOCI). La Escala de Yale-Brown para Niños (CY-BOCS) es de los instrumentos más frecuentemente utilizados en la clínica e investigación, que evalúan los tipos de obsesiones y compulsiones así como su severidad. La mayoría de los niños con TOC requieren múltiples tratamientos, por ejemplo: terapia cognitivo-conductual, fármacos, entrenamiento conductual para los familiares, etc. La disponibilidad de los inhibidores selectivos de la recaptura de serotonina (ISRS) ha cambiado sorprendentemente el tratamiento del TOC con efectividad basada en evidencia. Hasta el momento, se reconoce que la combinación de terapia cognitivo-conductual y tratamiento farmacológico con ISRS es la estrategia con mayores resultados y mejoría sostenida. <![CDATA[<b>Relación entre el consumo de tabaco, salud mental y malestares físicos en hombres trabajadores de una empresa textil mexicana</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400006&lng=es&nrm=iso&tlng=es Introduction Tobacco use is considered a worldwide public health problem because of the amount of death and disease it causes. The WHO reports that 30% of the adult population in the world are cigarette smokers, and that nearly five million of these will die within one year. Prospective studies performed by the WHO show that if current tobacco use continues, in 2020 there will be 8.4 million deaths due to tobacco-related diseases every year; seven out of 10 of these deaths will occur in emergent countries, like Mexico. More than 53000 tobacco users die every year in Mexico because of tobacco-related diseases, and at least 147 of these die daily. Data from the National Addictions Survey (NAS) 2002 showed that 26.4% of the people between 12 and 65 years old were active tobacco consumers; this amounted to nearly 14 million individuals. Of these, 7.1% were under 18 years old. The number of tobacco consumers in Mexico has increased from nine million in 1988 to 14 million in 2002. According to the NAS, 52% of the users smoke on a daily basis, and 61.4% of them began smoking when they were minors. To know the actual consumption levels, it is important to consider some factors: the number of cigarettes a person smokes, the different situations where a person smokes, and the social and physical consequences of smoking. Thus, it would be possible to develop a consumer classification (i. e. soft consumers, mild consumers, and hard consumers). There may be numerous causes for a person to be ill. When speaking about the harmful effects of tobacco use, the literature is clear in stating that these begin with the first cigarette smoked. However, it can take up to 30 years for a consumer to notice the damage on his health after his/her consumption began; but within the first ten years there are problems in lung function and in physical endurance. When a person starts smoking there are acute and unpleasant side effects that are rarely associated with smoked tobacco use. Consumption creates a tolerance which makes unpleasant effects to stop or fade away, giving place to pleasant sensations produced by nicotine; concentration improves and psychomotor skills, alert, and activation get better and there is a reduction in anxiety and stress. The relationship between tobacco use and mental health is evident at the level of the emotional outcomes of suffering a chronic illness, such as lung cancer. On the other hand, nicotine use has been related to a reduction in the severity of depression. Chemical alternatives for reducing consumption, based on the substance physical effects that promote addiction, have not proven to be effective so far. There is also evidence that consumers that fail in quitting smoking or people that have dependence problems with nicotine show a high prevalence of mayor depression when compared to non-dependent consumers. This association was direct with the severity of nicotine dependence. It also has been observed that smoking interferes often with psychological learning tools, mainly when consumption starts at very early ages. Emotional distress can produce low self-esteem and a lack of self-confidence. Therefore, the chances to begin tobacco consumption increase when it is used as a crutch to cope with social pressure and acceptance. Since tobacco use is a conduct that has shown to have serious repercussions on physical health and an important relationship with mental health in human beings, and is therefore a growing public health problem, the objective of this study is to explore a possible link among smoked tobacco consumption, mental health and physical problems in male workers from a textile factory. Method A non-probabilistic convenience sample was used in the study. Subjects voluntarily agreed to complete the questionnaire: 279 male workers were interviewed; 54% were between 18 and 27 years old and 23% were between 28 and 37. Most of them had studied junior high school or higher (74%) and 65% were in a serious relationship (married or living with a couple). Data about tobacco use were collected using a questionnaire with questions from the NAS 2002. To explore mental health the five-item Mental Health Inventory was used (MHI-5). As it is a self-answered screening test, it does not give a diagnosis, but it does allow establishing if subjects have symptoms of a probable mental health problem. Information about physical distress was collected through an 11-item somatization sub-scale from the Symptoms Check List-90 (SCL-90). The number of physical troubles that subjects reported during the last month was considered. All instruments have good levels of reliability and validity. Finally, several socio-demographic questions were included. The questionnaire was answered in groups inside a training room. Trained interviewers participated in the process of collecting information. Subjects' participation was voluntary and their verbal acceptation was obtained before answering the questionnaires. Anonymity and confidentiality were guaranteed. Workers were told that no information would be given to the union or business authorities, and those who asked for their results received them personally. Neither invasive procedures nor intervention techniques were used. The union authorities received a global report so they could acknowledge the importance of smoked tobacco and mental health-related problems among their workers. Statistical analyses were performed using SPSS 11.<hr/>Introducción El consumo de tabaco es considerado un problema de salud pública en todo el mundo debido a la cantidad de enfermedades y muertes relacionadas con su uso. La Organización Mundial de la Salud (OMS) reporta que 30% de los adultos son fumadores y, de éstos, aproximadamente cinco millones de personas morirán en un año. También se estima que para 2020 habrá 8.4 millones de muertes anuales por enfermedades relacionadas con el consumo de tabaco, de las cuales siete de cada 10 ocurrirán en países en vías de desarrollo, como México, donde más de 53 mil personas fumadoras mueren al año por enfermedades asociadas al tabaquismo y al menos 147 personas mueren diariamente. Por otro lado, en la bibliografía se ha encontrado que el daño en el organismo por fumar comienza desde el primer cigarro, que a los 10 años se presentan síntomas sutiles en la función pulmonar y disminución de la tolerancia al ejercicio, y que es entre 20 y 30 años después cuando los síntomas hacen a un fumador tomar conciencia del daño a su salud. En cuanto a la relación entre el uso de tabaco y la salud mental, ésta se evidencia por las consecuencias emocionales que conlleva padecer una enfermedad crónica. En este contexto, el objetivo del presente trabajo fue conocer la relación de problemas emocionales y malestares físicos con el consumo de tabaco en hombres trabajadores de una empresa textil mexicana. Método La muestra estuvo conformada por 279 sujetos que laboraban en una empresa textil, en su mayoría jóvenes entre 18 y 27 años (54.5%), con escolaridad de secundaria (59.3%) y casados o en unión libre (65.6%). El instrumento utilizado incluyó las escalas de salud mental (MHI-5), malestares físicos (SCL-90) y consumo de tabaco. La aplicación del instrumento se realizó de manera grupal dentro de la empresa textil en que laboraban los sujetos. Resultados No se encontraron diferencias significativas en cuanto a problemas de salud mental y síntomas físicos entre fumadores y no fumadores. Mediante un modelo de análisis de trayectorias, se analizó la relación existente entre síntomas físicos, problemas de salud mental e indicadores de consumo de tabaco. Se encontró así que el principal predictor de los síntomas físicos en fumadores es el tiempo que llevan consumiendo y que los síntomas físicos son un importante predictor de problemas de salud mental. Discusión Sin importar la cantidad de cigarrillos consumidos, la frecuencia de consumo ni otros indicadores de consumo elevado, el tiempo que se lleva consumiendo es un predictor importante del número de síntomas físicos que se manifiestan, lo que puede deberse a los efectos dañinos que tiene el consumo prolongado del tabaco. De este modo se confirma lo mencionado en otras investigaciones de que, después de los primeros 10 años de consumo, se presentan malestares físicos sutiles y que a lo largo de 20 o 30 años se presentaran malestares importantes. Si bien no se encontró una relación directa entre consumo de tabaco y salud mental, se puede sugerir una relación indirecta derivada de la influencia que tiene el consumo sobre el plano del bienestar físico. En este sentido es de esperarse que, a medida que se continúe consumiendo tabaco y los malestares físicos aumenten, también se incrementen los problemas de salud mental. Por otro lado, el modelo aquí presentado requiere ser completado incluyendo otras áreas que puedan influir sobre el bienestar físico y mental. Sin embargo, se logró evidenciar la importancia que tiene el consumo de tabaco sobre el malestar físico, a la vez que aumenta la probabilidad de que se presenten más problemas en la salud mental de la población consumidora. <![CDATA[<b>Estudio controlado doble-ciego con clonazepam y placebo en pacientes con trastorno de ansiedad social</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400007&lng=es&nrm=iso&tlng=es Introduction Social anxiety disorder or social phobia affects approximately 4.7% of the general population as shown in Mexican epidemiological studies and studies done in other countries. The symptoms of this disorder are more frequent in women (5.4%) than in men (3.8%) and younger people (18 to 29 years), with an average onset age of 13 years. The main clinical characteristic of social phobia is an intense and irrational fear to be exposed to social situations. Social phobia emerges to anticipate or be submitted into situations where the subject could be evaluated or be observed by others. Treatment of social phobia is important because this disorder has been associated with an increase rate of suicidal intents, financial dependency and psychiatric comorbidity. Pharmacological treatment of social phobia includes SSRI and MAOI antidepressants and benzodiacepines. For the treatment of social phobia, potent benzodiacepines, such as alprazolam and clonazepam, have showed efficacy in several studies. In 1993 Davidson et al. published the first double-blind controlled study with clonazepam in patients with social phobia. They found that patients using clonazepam showed an improvement from the first week of treatment and that improvement persisted during the study and was superior to placebo. The objective of the present study was to improve our knowledge about the efficacy and tolerability of clonazepam in patients with social phobia. We studied a group of social phobic patients during 24 weeks in a double-blind treatment study with clonazepam and placebo. Patients took one week single-blind of placebo, followed by 16 weeks of double-blind treatment with clonazepam or placebo. During the first six weeks of the double-blind treatment, dosage was adjusted looking for maximal improvement and tolerability. After this phase we selected only those patients who improved and they were treated double-blind for 10 more weeks with clonazepam or placebo. Discontinuation of treatment was done in a period of two weeks during which clonazepam was changed to placebo and then patients followed with a four weeks of single-blind treatment with placebo. Methods All patients signed consent forms for the study which was approved by our hospital Ethical Committee. Patients were selected from those who looked for help in our Anxiety and Depression Research Clinic or by newspaper advertising. All candidate patients were interviewed with the SCID-I Anxiety Disorders section for DSM-III-R diagnosis of social phobia. Also, patients had to rank in the PARS scale a higher score in the Social phobia section than in the Separation phobia section. Also, patients included had to have at least a moderate severity of social anxiety disorder. Exclusion criteria required that patients had not had any other psychiatric disorders, including psychotic disorders, bipolar disorder, major depression, history of abuse or addiction to alcohol or drugs, eating disorders and anxiety disorders as panic disorder, generalized anxiety disorder, obsessive-compulsive disorder and post-traumatic stress disorder. Also, patients needed to be free of any psychotropic medication. A two week of discontinuation phase was conducted with patients receiving benzodiacepines or antidepressants (six weeks for fluoxetine). From a total of 85 patients (78% males and 22% females), 62 were admitted in the fist single-blind week of placebo. Mean age of patients included (± DS) was 28.17 (8.95) years (79 % male and 79% single). Of them, nine patients (14.5%) showed a placebo response and were not admitted to the double-blind treatment phase. A clinical evaluation of the patients was carried out on each visit with the Clinical Global Impression of severity and improvement of eight points for the Global severity of social phobia, Anticipatory anxiety and Phobic avoidance, the Hamilton anxiety and COVI scales, the Liebowitz Social Phobic Disorder Rating Form (LSPD) and the Hamilton depression and Raskin scales. Also, patients completed on each visit the Global impression of severity and improvement of 8 points, the Liebowitz social anxiety scale (LSAS), the Marks' fear questionnaire and an Incapacity score. Patients were evaluated each week for the first four weeks of double-blind treatment and later each two weeks.<hr/>Resumen Introducción El trastorno de ansiedad social o fobia social afecta a 4.7% de la población, de acuerdo con reportes epidemiológicos de México y otros países. Los síntomas de este trastorno son más frecuentes en la mujer (5.4%) que en el hombre (3.8%) y en personas jóvenes (18 a 29 años) con una edad de inicio de 13 años. El tratamiento de la fobia social es importante ya que este padecimiento se asocia con comorbilidad psiquiátrica, abuso y dependencia de sustancias, mayor incidencia de intentos suicidas y dependencia financiera. Entre los tratamientos farmacológicos para este trastorno contamos con antidepresivos del tipo ISRS e IMAO y benzodiacepinas. En 1993 Davidson et al. publicaron el primer estudio doble-ciego controlado con placebo y clonazepam en el tratamiento de la fobia social. Los autores encontraron que el clonazepam mejoraba a los pacientes desde la primera semana de tratamiento. Nosotros estudiamos la efectividad y tolerabilidad del clonazepam en pacientes con fobia social en un estudio de 24 semanas, doble-ciego con asignación al azar, controlado contra placebo. Este estudio incluyó una fase simple-ciego de tratamiento con placebo de una semana, 16 semanas de tratamiento doble-ciego con clonazepam o placebo y una fase final de discontinuación con placebo simple-ciego. Material y métodos El diagnóstico de fobia social se estableció de acuerdo con la sección de trastornos de ansiedad del SCID-I para establecer el diagnóstico de acuerdo a los criterios del DSM-III-R. Se incluyeron 62 pacientes en la fase simple-ciego, 53 de los cuales ingresaron a la fase doble-ciego del estudio por no haber mejorado. Las evaluaciones clínicas se realizaron con las escalas ICG de severidad y de mejoría de 8 puntos para la Enfermedad global, Ansiedad anticipatoria y Evitación fóbica, las escalas HamA y Covi, Liebowitz Social Phobic Disorder Rating Form (LSPD), HamD y de Raskin. Los pacientes completaron la ICG-S y la ICG-M de 8 puntos, la escala de Liebowitz para ansiedad social (LSAS), la escala de miedos de Marks y la escala de incapacidad. Resultados En la fase doble-ciego del estudio 27 pacientes recibieron placebo y 26, clonazepam. A la fase de seguimiento doble-ciego de 10 semanas entraron sólo los pacientes que mejoraron, 20 en clonazepam (73%) y siete en placebo (25.9%). Las evaluaciones clínicas fueron realizadas cada semana durante las primeras cuatro semanas y cada dos semanas posteriormente. El análisis de las evaluaciones clínicas al punto final del tratamiento mostró un mayor beneficio en los pacientes que recibieron clonazepam que aquellos que estuvieron con placebo (ANOVA p=.001). En la escala ICG de mejoría las respuestas «muy mejorado» y «mucho muy mejorado» al final del tratamiento se observaron en 65.3% (N=17) de los pacientes con clonazepam y en 29.6% (N=8) de pacientes con placebo. Con clonazepam se observó mejoría desde la segunda semana del tratamiento (ANOVA p=.001). La razón más frecuente para no completar el estudio fue la respuesta clínica insuficiente (19% en clonazepam n=5 y 66.6% en placebo n=18; P=.001), abandono del tratamiento (NS) y experiencias adversas (NS). La dosis final de clonazepam fue de 3.4±DS 2.27 mg/día. Se presentaron más eventos adversos con clonazepam (3.85 ± 3.13) que con placebo (0.81 ± 1.08) (p<.0001). Cuatro pacientes de 16 (25%) en clonazepam que iniciaron la fase de supresión abandonaron el estudio por síndromes de supresión del medicamento. Discusión Nuestro estudio corrobora los hallazgos del primer estudio controlado de Davidson et al., de 1993, y datos de numerosos estudios abiertos en el sentido de que el clonazepam es un tratamiento rápido y eficaz para el trastorno de ansiedad social. Nuestro estudio aporta también datos sobre la prevalencia de sucesos adversos y síntomas de supresión y recaídas tempranas al retirar el clonazepam hasta en 25% de pacientes. Las benzodiacepinas pueden estar contraindicadas en grupos de pacientes con patología comórbida y aquellos que abusan o son adictos al alcohol y las drogas. En tales casos la terapia cognoscitivo-conductual acompañada de medicamentos antidepresivos del tipo ISRS o IMAO puede ser una mejor opción de tratamiento primario para la fobia social. <![CDATA[<b>Los antidepresivos inhibidores selectivos de recaptura de serotonina (ISRS, ISR-5HT)</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400008&lng=es&nrm=iso&tlng=es Depression is a frequent mental disorder in the general population. Approximately 3.7% of the population will suffer a major depressive episode throughout life. Pharmacological treatment with selective serotonin receptor inhibitors (SSRIs) is useful to treat this condition and other mental disorders. Citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine and sertraline, which constitute this group, are characterized by having an easy way of administration and a very extensive security profile. Objectives The objectives in this revision were: 1. To establish current indications of selective serotonin receptor inhibitors, using as basis those authorized by the Food and Drug Administration (FDA) of the United States of America. 2. To describe the mechanisms that explain antidepressant action. Initially, the SSRIs inhibit the reuptake of serotonin at the synaptic cleft; later there is a downregulation of the 5HT1A receptors; and finally antidepressants raise the levels of brain derived neurotrophic factor (BDNF). 3. To present its way of administration and dosage. 4. To describe frequent collateral effects and those specifically associated to this group of antidepressants and the recommended treatment. Results SSRIs antidepressants are the first choice treatment in depression, in the anxiety disorder, the obsessive-compulsive disorder, the post-traumatic stress disorder, bulimia nervosa and the premenstrual dysphoric disorder. At present, SSRIs displace benzodiacepines in the treatment of generalized anxiety disorder, just as they displaced tricyclic antidepressants in the past. Depressed patients show less activity than normal of the serotonin neurotransmitter (serotonergic hypothesis of depression) and the reuptake blockade at the site of the serotonergic presinaptic receptors 5HT1A, 5HT2C and 5HT3C increases neurotransmission in this system. Desensitization of autoreceptors 5HT1A and the downregulation of the 5HT2 receptors coupled to the G protein, a late effect of the SSRIs, result in the improvement of the depressive symptoms. The mechanism that explains the relatively late antidepressant effect seems to be different to the acute and fast serotonergic effect responsible of improvement in the premenstrual dysphoric disorder. Moreover, these antidepressants, in the same way than mood stabilizers and electroconvulsive therapy, increase serum levels of the brain-derived neuronal growth factor, as well as other neurotrophic factors. Although the SSRIs dosages are variable, it is possible to start antidepressant treatment with therapeutic doses in the majority of cases; at the same time, if necessary, it is possible to augment them gradually up to the largest dose, with a wide security margin. Their most frequent collateral effects occur in the gastrointestinal system, in the sexual response and on bone density. Nevertheless, there are collateral effects specifically related to the use of these antidepressant medications: 1. The serotonergic syndrome, characterized by changes in the mental status, autonomic hyperactivity and neuromuscular anomalies. 2. The syndrome of inappropriate secretion of antidiuretic hormone, which occurs in 25% of the elder depressed patients treated, and which is characterized by a high serum osmolarity, low urinary osmolarity and hyponatremia. Its manifestations are malaise, myalgias, drowsiness and headache, but it may produce also confusion, convulsions and coma. 3. Gastrointestinal bleeding mainly and cutaneous bleeding: Use of SSRIs raises 2 to 4 times the risk of bleeding. When the patient takes aspirin it is raised up to 7 times, and with the concomitant use of anti-inflammatory drugs, by nearly 16 times. Other risk factors are age, the antecedent of bleeding and the potency of SSRIs to inhibit the serotonin reuptake. 4. The discontinuation syndrome, lesser with fluoxetine, and greater with paroxetine and sertraline. It appears by the second day and it lasts two weeks. Its manifestations are nausea, headache, paresthesias, nasal congestion and general malaise. They are due to the decrease in serotonin levels at the synaptic cleft. 6. Effects on the newborn when the SSRIs are used during pregnancy consist in specific congenital malformations. Sertraline has been associated to omphalocele, ventricular septum heart defects and anencephaly. Fluoxetine is associated to craniosynostosis and paroxetine to heart defects, gastroschisis, neural tube defects, omphalocele and anencephaly also. Its use also increases the range of spontaneous abortions up to 1.45 times, premature delivery and low birth weight, problems in the early newborn period (respiratory problems and hypotony), hypoglycemia, cyanosis, restlessness, convulsions and low Apgar. Its use during the third trimester can cause persistent lung hypertension. Although it is a rare condition, it is associated to a mortality range of 10% to 20%. 8) Little is known about the effects caused by the use of SSRIs during breastfeeding. In the case of sertraline and paroxetine, these antidepressant drugs are not detected in the child's serum; on the other hand, serum levels of citalopram were 1.9 nmol/L, fluoxetine 47 nmol/L, and venlafaxine 91 nmol/L. In the available studies, neither behavioral effects nor effects in the development of the newborn were observed. 9) Suicide risk or suicidality. Although the antidepressant treatment lowers both, ideation and the frequency of suicides in the patients treated, the FDA has established a series of general recommendations for the management of patients who start the treatment with antidepressants. To start with the lowest dose, to make an appointment weekly during six consecutive weeks, to recommend and facilitate contact via telephone, to prohibit the use of alcohol and drugs, to ask on each date about suicidal thoughts or behaviors or about self-mutilation, to document the information in the file and to use supportive psychotherapy or cognitive, behavioral or interpersonal therapies.<hr/>La depresión es un trastorno mental que afecta a 3.7 % de la población. Los antidepresivos inhibidores selectivos de la recaptura de serotonina (ISRS) resultan útiles en el tratamiento de éste y otros trastornos mentales. El citalopram, escitalopram, fluoxetina, fluvoxamina, paroxetina y sertralina constituyen este grupo de fácil administración y con un amplio perfil de seguridad. Objetivos 1) Establecer las indicaciones actuales de los antidepresivos ISRS. 2) Describir los mecanismos que explican su acción antidepresiva. 3) Describir los efectos secundarios frecuentes y aquéllos específicamente relacionados con este grupo antidepresivo. Resultados Los antidepresivos ISRS son el tratamiento de elección para la depresión, los trastornos de angustia, de ansiedad generalizada, obsesivo-compulsivo, de estrés postraumático, disfórico premenstrual y la bulimia nervosa. Los pacientes deprimidos muestran una actividad menor a la normal del neurotransmisor serotonina. La inhibición de la recaptura de la serotonina sobre los receptores serotoninérgicos presinápticos 5HT1A, 5HT2C y 5HT3C aumenta la neurotransmisión en este sistema. La desensibilización de los autorreceptores 5HT1A y la regulación hacia abajo (downregulation) de los receptores 5HT2 acoplados a la proteína G, efecto tardío de los ISRS, dan por resultado la mejoría de los síntomas depresivos. El mecanismo que explica el efecto antidepresivo relativamente tardío parece ser distinto al efecto serotoninérgico agudo y rápido responsable de la mejoría en el caso del trastorno disfórico premenstrual. Estos antidepresivos, como los estabilizadores del ánimo y la terapia electroconvulsiva, incrementan los niveles séricos del factor de crecimiento neuronal cerebral, así como de otros factores neurotróficos. Aunque las dosis de los ISRS son variables, en la mayoría de los casos es posible iniciar el tratamiento antidepresivo con dosis terapéuticas e incrementarlas paulatinamente hasta las dosis máximas con seguridad. Sus efectos secundarios más frecuentes son gastrointestinales, en la respuesta sexual y sobre la densidad ósea. Los efectos secundarios específicamente relacionados con el uso de estos antidepresivos son: 1. El síndrome serotoninérgico, caracterizado por cambios en el estado mental, hiperactividad autonómica y anomalías neuromusculares. 2. El síndrome de secreción inapropiada de hormona antidiurética, que se caracteriza por osmolaridad sérica alta, urinaria baja e hiponatremia, así como por mialgias, letargo, cefalea e incluso confusión, convulsiones y coma. 3. El sangrado, principalmente de tubo digestivo y cutáneo. El uso de los ISRS aumenta el riesgo de sangrar entre dos y cuatro veces. Cuando el paciente usa aspirina, el riesgo aumenta hasta siete veces y con el uso concomitante de antiinflamatorios, cerca de 16 veces. La edad, el antecedente de sangrado y la capacidad de inhibir la recaptura constituyen también factores de riesgo. 4. El síndrome de descontinuación, menor con la fluoxetina, mayor con la paroxetina y sertralina, aparece a partir del segundo día y su duración es de dos semanas. Manifestaciones como náusea, cefalea, parestesias, congestión nasal y malestar general se deben a la disminución de los niveles de serotonina en la sinapsis. 5. Los efectos sobre el producto cuando los ISRS se utilizan durante la gestación consisten en malformaciones congénitas específicas. La sertralina se ha asociado a onfalocele, defectos del septum cardíaco y anencefalia. A su vez, la fluoxetina se ha asociado a craneosinostosis y defectos cardíacos. Y la paroxetina a defectos cardíacos, gastrosquisis, defectos del tubo neural y también a onfalocele y anencefalia. Su uso también aumenta la tasa de abortos espontáneos hasta 1.45 veces, parto prematuro y bajo peso al nacer, problemas en el neonato inmediato (problemas respiratorios e hipotonía), hipoglucemia, cianosis, inquietud, convulsiones y Apgar bajo. Su uso durante el tercer trimestre puede ocasionar hipertensión pulmonar persistente que, aunque es rara, se asocia a una mortalidad de 10- 20 %. 6) De los efectos por el uso de ISRS durante la lactancia se conoce poco. En el caso de la sertralina y la paroxetina no se detectan estos antidepresivos en el suero del niño; en cambio, los niveles séricos de citalopram fueron de 1.9 nmol/L, de fluoxetina 47 nmol/L y de venlafaxina de 91 nmol/ L. En los estudios disponibles no se observaron efectos conductuales o en el desarrollo del recién nacido. 7) Suicidalidad o riego suicida. Aunque el tratamiento antidepresivo disminuye tanto la ideación y la frecuencia de suicidios en los pacientes tratados, la FDA ha establecido una serie de recomendaciones para el manejo de pacientes que inician el tratamiento con antidepresivos ISRS: Iniciar con la dosis más baja, citar semanalmente a los pacientes durante 6 semanas consecutivas, recomendar y facilitar el contacto telefónico, prohibir el uso de alcohol y drogas, interrogar en cada ocasión sobre pensamientos y comportamientos suicidas o autolesivos, documentar en el expediente la información y usar psicoterapia de apoyo, cognitivo-conductual o interpersonal en el tratamiento. <![CDATA[<b>El suicidio y algunos de sus correlatos neurobiológicos. </b><b>Primera parte</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400009&lng=es&nrm=iso&tlng=es Suicidal behavior is a complex and multifactorial phenomenon. At present, growing evidence shows the participation of biological traits in suicidality. Some findings suggest the dysfunction of the serotonin system, since serotonin and some of its receptor subtypes are involved in the modulation of such as affective behavior and cognition, among other behavioral processes. The content of 5-hydroxyindoleacetic acid, the major serotonin metabolite, is reduced in the cerebrospinal fluid of violent suicide attempters, independently of any other previous psychiatric diagnosis. In fact, this reduction may predict future suicide attempts and suicide completion. Post-mortem studies of ventromedial prefrontal cortex from suicide victims show decreased density of the 5-HT1A presynaptic serotonergic receptor subtype, and a compensatory upregulation of the 5-HT2A serotonergic post-synaptic receptor subtype. These observations on suicide strongly suggest a role of the two serotonin receptor subtypes located in this cortical brain region. Dysfunction of this region may support the diathesis concept (vulnerability) associated to suicidal behavior. In fact, some people display impulsive and self-aggressive behavior as part of their suicidality. This dysfunction is associated with alterations in the polymorphisms of tryptophan hydroxylase gene expression, i.e., the rate-limiting enzyme which in turn modifies the biosynthesis of serotonin, contributing to the reduction of serotonergic activity. Since the prefrontal cortex and related structures play a major role in mood regulation, their participation in the pathophysiology of affective disorders and suicide is currently being discussed. A circuit integrated by prefrontal cortex, hippocampus, amygdaloid complex, lateral septal nucleus and other functionally related structures could be involved in the regulation of emotional memory, hedonism and decision-taking. The hippocampus is implicated in cognition and is one of the cerebral structures strongly affected by stress. Structural abnormalities in cortical and hippocampal areas and reduced hippocampal plasticity have been demonstrated in patients suffering from chronic stress and affective disorders. Reduced neurotrophin expression may be associated with structural abnormalities and reduced hippocampal plasticity. A decrease in the content of neurotrophins in the prefrontal cortex and hippocampus could be of relevance in suicidal behavior. Human post-mortem studies supported by living animals studies have demonstrated that antidepressants increase the activity of the brain-derived neurotrophic factor (BDNF) and increase the density of its receptor (BDNF-tyrosine kinase receptor B: trkB), which seems to participate in the therapeutic effects of drugs used in the treatment of depression. On the contrary, the reduction of BNDF trkB-receptor mRNA has been related to suicidal behavior, since a reduction of plasma BNDF levels has been reported in major depression. BNDF levels have also been suggested as a biological marker of suicidal depression. Abnormalities in the ventromedial prefrontal cortex in suicidal individuals largely correlate with the neurochemical deficits reported in this population. In fact, prefrontal hypofunction and impaired serotonergic responsivity are proportional to the lethality of the suicide attempt. Positron emission tomographic studies indicate lower ventromedial prefrontal cortex activity, behaviorally associated with high impulsivity, higher planning of suicidal intent, and higher-lethality suicide attempts. Other studies have also related structural abnormalities in amygdala with suicidality. The function of this region is critical regarding fear, anxiety, aggression and the recognition and response to danger, i.e., some behavioral patterns involved in suicidality. Anxiety commonly follows or precedes depression. Therefore, amygdaline dysfunction may increase the risk of suicidal behavior. For depressive-suicide attempters, the suicide act itself occurs at a moment of extreme anxiety, strongly suggesting amygdaloid complex participation in the process. Lastly, the lateral septal nucleus is related with anhedonia and hopelessness (despair). Since its neuronal firing rate increases after the experimental application of clinically effective antidepressant treatments. The septal nucleus is considered a target of these drugs, a suggestion supported by the observation that anhedonia is one of the main symptoms in depression and lateral septal nucleus activity is involved in hedonic process. Anhedonia, hopelessness and other depressive symptoms are significantly related to suicidal ideation. Taking into account that some patients with major depression are vulnerable to suicide, this vulnerability may result from the interaction of suicidality with environmental precipitants and a lowered threshold for suicidal behavior. Certainly, one of the psychiatric disorders associated with suicide is depression, which suggests a causal relationship and suggests the involvement of these brain structures in suicidality.<hr/>El suicidio es un fenómeno complejo y multifactorial. A pesar de que varios de los factores de riesgo ya han sido identificados, las bases neurobiológicas del suicidio no se han esclarecido del todo, aunque se han enfocado particularmente hacia la disfunción del sistema serotonérgico. Los primeros estudios indicaban que, en sujetos con intentos suicidas, se encuentran niveles reducidos del ácido 5-hidroxiindol-acético, principal metabolito de la serotonina, en el líquido cefalorraquídeo, independientemente del diagnóstico psiquiátrico previo. Más adelante, algunos estudios post-mortem han identificado alteraciones en los receptores presinápticos (5-HT1A) y postsinápticos (5-HT2A, 5-HT1A) de la corteza prefrontal ventromedial. Esta disfunción, al parecer, se asocia con alteraciones en los genes que codifican la expresión de enzimas implicadas en la síntesis y metabolismo de la serotonina, aunada a una alteración en la expresión genética de factores neurotróficos derivados del cerebro, los cuales intervienen en la regulación funcional de las neuronas serotonérgicas. En conjunto, estas alteraciones se han relacionado con la vulnerabilidad o la diátesis para el comportamiento suicida en individuos con predisposición a la conducta violenta e impulsiva o autoagresiva. Además, confluye una hiperactividad del eje hipotálamo-hipófisis-adrenal, confirmada por un incremento de la hormona adrenocorticotrófica y una reducción del número de receptores para esta hormona en la corteza prefrontal de suicidas. La corteza prefrontal desempeña un papel fundamental en la regulación del estado de ánimo y se le ha implicado tanto en la fisiopatología de los trastornos afectivos como en el suicidio. Por medio de estudios con tomografía por emisión de positrones, se determinó que en los sujetos con intento de suicidio existe una hipofuncionalidad de la corteza prefrontal ventromedial, lo cual se ha asociado con la impulsividad y la planeación para intentar suicidarse. Asimismo, el hipocampo se ha implicado en la cognición y es una estructura que participa en el estrés, un factor predisponente al suicidio. Algunos sistemas celulares también han sido implicados, por ejemplo, los factores de transcripción CREB (proteína ligada al AMP cíclico), los cuales están disminuidos en la corteza prefrontal, hipocampo y amígdala de suicidas. Algunos otros estudios sugieren incluso anormalidades estructurales en la amígdala. Aunque es especulativo proponer que la amígdala cumpla un papel específico en el suicidio, tal propuesta no carece de bases dado que esta región es crítica en la integración de la ansiedad y en la agresión, además de que guía las respuestas apropiadas que deben emitirse bajo situaciones de peligro. Por otro lado, el núcleo septal lateral se ha implicado en la desesperanza y en las acciones de diversos tratamientos antidepresivos. Entonces, se puede integrar un circuito anatómico y funcional en el cual participan como entrada los sistemas sensoriales, de ahí a estructuras integradoras de la memoria emocional, ubicadas principalmente en el lóbulo temporal, para de ahí pasar a estructuras de la neocorteza, principalmente la corteza prefrontal, mediante las proyecciones de núcleos talámicos. Esta vía integra la percepción del ambiente, información que es contrastada en los circuitos de la memoria emocional, para de ahí pasar a la toma de decisiones. Las alteraciones funcionales de este circuito, aunadas a factores ambientales adversos, parecen promover el acto suicida. En fin, en el suicidio participan estructuras cerebrales integradoras del estado afectivo, la memoria emocional, la impulsividad y la toma de decisiones. Quizá por todo ello, aunque se acepta la eficacia de los antidepresivos, del litio y de los antipsicóticos de segunda generación, se cuestiona aún la eficacia de los antipsicóticos convencionales, por su escasa acción en el estado afectivo. Aunque la depresión es una entidad clínica de riesgo para el suicidio, no es la única, pues también son factores de riesgo el trastorno bipolar y el trastorno esquizoafectivo. Cualquiera de ellos, aunado a agitación e impulsividad, debe llamar la atención para seleccionar el tratamiento farmacológico preventivo pertinente. <![CDATA[<b>Dionisio Nieto y la investigación científica</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400010&lng=es&nrm=iso&tlng=es Suicidal behavior is a complex and multifactorial phenomenon. At present, growing evidence shows the participation of biological traits in suicidality. Some findings suggest the dysfunction of the serotonin system, since serotonin and some of its receptor subtypes are involved in the modulation of such as affective behavior and cognition, among other behavioral processes. The content of 5-hydroxyindoleacetic acid, the major serotonin metabolite, is reduced in the cerebrospinal fluid of violent suicide attempters, independently of any other previous psychiatric diagnosis. In fact, this reduction may predict future suicide attempts and suicide completion. Post-mortem studies of ventromedial prefrontal cortex from suicide victims show decreased density of the 5-HT1A presynaptic serotonergic receptor subtype, and a compensatory upregulation of the 5-HT2A serotonergic post-synaptic receptor subtype. These observations on suicide strongly suggest a role of the two serotonin receptor subtypes located in this cortical brain region. Dysfunction of this region may support the diathesis concept (vulnerability) associated to suicidal behavior. In fact, some people display impulsive and self-aggressive behavior as part of their suicidality. This dysfunction is associated with alterations in the polymorphisms of tryptophan hydroxylase gene expression, i.e., the rate-limiting enzyme which in turn modifies the biosynthesis of serotonin, contributing to the reduction of serotonergic activity. Since the prefrontal cortex and related structures play a major role in mood regulation, their participation in the pathophysiology of affective disorders and suicide is currently being discussed. A circuit integrated by prefrontal cortex, hippocampus, amygdaloid complex, lateral septal nucleus and other functionally related structures could be involved in the regulation of emotional memory, hedonism and decision-taking. The hippocampus is implicated in cognition and is one of the cerebral structures strongly affected by stress. Structural abnormalities in cortical and hippocampal areas and reduced hippocampal plasticity have been demonstrated in patients suffering from chronic stress and affective disorders. Reduced neurotrophin expression may be associated with structural abnormalities and reduced hippocampal plasticity. A decrease in the content of neurotrophins in the prefrontal cortex and hippocampus could be of relevance in suicidal behavior. Human post-mortem studies supported by living animals studies have demonstrated that antidepressants increase the activity of the brain-derived neurotrophic factor (BDNF) and increase the density of its receptor (BDNF-tyrosine kinase receptor B: trkB), which seems to participate in the therapeutic effects of drugs used in the treatment of depression. On the contrary, the reduction of BNDF trkB-receptor mRNA has been related to suicidal behavior, since a reduction of plasma BNDF levels has been reported in major depression. BNDF levels have also been suggested as a biological marker of suicidal depression. Abnormalities in the ventromedial prefrontal cortex in suicidal individuals largely correlate with the neurochemical deficits reported in this population. In fact, prefrontal hypofunction and impaired serotonergic responsivity are proportional to the lethality of the suicide attempt. Positron emission tomographic studies indicate lower ventromedial prefrontal cortex activity, behaviorally associated with high impulsivity, higher planning of suicidal intent, and higher-lethality suicide attempts. Other studies have also related structural abnormalities in amygdala with suicidality. The function of this region is critical regarding fear, anxiety, aggression and the recognition and response to danger, i.e., some behavioral patterns involved in suicidality. Anxiety commonly follows or precedes depression. Therefore, amygdaline dysfunction may increase the risk of suicidal behavior. For depressive-suicide attempters, the suicide act itself occurs at a moment of extreme anxiety, strongly suggesting amygdaloid complex participation in the process. Lastly, the lateral septal nucleus is related with anhedonia and hopelessness (despair). Since its neuronal firing rate increases after the experimental application of clinically effective antidepressant treatments. The septal nucleus is considered a target of these drugs, a suggestion supported by the observation that anhedonia is one of the main symptoms in depression and lateral septal nucleus activity is involved in hedonic process. Anhedonia, hopelessness and other depressive symptoms are significantly related to suicidal ideation. Taking into account that some patients with major depression are vulnerable to suicide, this vulnerability may result from the interaction of suicidality with environmental precipitants and a lowered threshold for suicidal behavior. Certainly, one of the psychiatric disorders associated with suicide is depression, which suggests a causal relationship and suggests the involvement of these brain structures in suicidality.<hr/>El suicidio es un fenómeno complejo y multifactorial. A pesar de que varios de los factores de riesgo ya han sido identificados, las bases neurobiológicas del suicidio no se han esclarecido del todo, aunque se han enfocado particularmente hacia la disfunción del sistema serotonérgico. Los primeros estudios indicaban que, en sujetos con intentos suicidas, se encuentran niveles reducidos del ácido 5-hidroxiindol-acético, principal metabolito de la serotonina, en el líquido cefalorraquídeo, independientemente del diagnóstico psiquiátrico previo. Más adelante, algunos estudios post-mortem han identificado alteraciones en los receptores presinápticos (5-HT1A) y postsinápticos (5-HT2A, 5-HT1A) de la corteza prefrontal ventromedial. Esta disfunción, al parecer, se asocia con alteraciones en los genes que codifican la expresión de enzimas implicadas en la síntesis y metabolismo de la serotonina, aunada a una alteración en la expresión genética de factores neurotróficos derivados del cerebro, los cuales intervienen en la regulación funcional de las neuronas serotonérgicas. En conjunto, estas alteraciones se han relacionado con la vulnerabilidad o la diátesis para el comportamiento suicida en individuos con predisposición a la conducta violenta e impulsiva o autoagresiva. Además, confluye una hiperactividad del eje hipotálamo-hipófisis-adrenal, confirmada por un incremento de la hormona adrenocorticotrófica y una reducción del número de receptores para esta hormona en la corteza prefrontal de suicidas. La corteza prefrontal desempeña un papel fundamental en la regulación del estado de ánimo y se le ha implicado tanto en la fisiopatología de los trastornos afectivos como en el suicidio. Por medio de estudios con tomografía por emisión de positrones, se determinó que en los sujetos con intento de suicidio existe una hipofuncionalidad de la corteza prefrontal ventromedial, lo cual se ha asociado con la impulsividad y la planeación para intentar suicidarse. Asimismo, el hipocampo se ha implicado en la cognición y es una estructura que participa en el estrés, un factor predisponente al suicidio. Algunos sistemas celulares también han sido implicados, por ejemplo, los factores de transcripción CREB (proteína ligada al AMP cíclico), los cuales están disminuidos en la corteza prefrontal, hipocampo y amígdala de suicidas. Algunos otros estudios sugieren incluso anormalidades estructurales en la amígdala. Aunque es especulativo proponer que la amígdala cumpla un papel específico en el suicidio, tal propuesta no carece de bases dado que esta región es crítica en la integración de la ansiedad y en la agresión, además de que guía las respuestas apropiadas que deben emitirse bajo situaciones de peligro. Por otro lado, el núcleo septal lateral se ha implicado en la desesperanza y en las acciones de diversos tratamientos antidepresivos. Entonces, se puede integrar un circuito anatómico y funcional en el cual participan como entrada los sistemas sensoriales, de ahí a estructuras integradoras de la memoria emocional, ubicadas principalmente en el lóbulo temporal, para de ahí pasar a estructuras de la neocorteza, principalmente la corteza prefrontal, mediante las proyecciones de núcleos talámicos. Esta vía integra la percepción del ambiente, información que es contrastada en los circuitos de la memoria emocional, para de ahí pasar a la toma de decisiones. Las alteraciones funcionales de este circuito, aunadas a factores ambientales adversos, parecen promover el acto suicida. En fin, en el suicidio participan estructuras cerebrales integradoras del estado afectivo, la memoria emocional, la impulsividad y la toma de decisiones. Quizá por todo ello, aunque se acepta la eficacia de los antidepresivos, del litio y de los antipsicóticos de segunda generación, se cuestiona aún la eficacia de los antipsicóticos convencionales, por su escasa acción en el estado afectivo. Aunque la depresión es una entidad clínica de riesgo para el suicidio, no es la única, pues también son factores de riesgo el trastorno bipolar y el trastorno esquizoafectivo. Cualquiera de ellos, aunado a agitación e impulsividad, debe llamar la atención para seleccionar el tratamiento farmacológico preventivo pertinente. <![CDATA[<b>José Luis Díaz. <i>La conciencia viviente</i></b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400011&lng=es&nrm=iso&tlng=es Suicidal behavior is a complex and multifactorial phenomenon. At present, growing evidence shows the participation of biological traits in suicidality. Some findings suggest the dysfunction of the serotonin system, since serotonin and some of its receptor subtypes are involved in the modulation of such as affective behavior and cognition, among other behavioral processes. The content of 5-hydroxyindoleacetic acid, the major serotonin metabolite, is reduced in the cerebrospinal fluid of violent suicide attempters, independently of any other previous psychiatric diagnosis. In fact, this reduction may predict future suicide attempts and suicide completion. Post-mortem studies of ventromedial prefrontal cortex from suicide victims show decreased density of the 5-HT1A presynaptic serotonergic receptor subtype, and a compensatory upregulation of the 5-HT2A serotonergic post-synaptic receptor subtype. These observations on suicide strongly suggest a role of the two serotonin receptor subtypes located in this cortical brain region. Dysfunction of this region may support the diathesis concept (vulnerability) associated to suicidal behavior. In fact, some people display impulsive and self-aggressive behavior as part of their suicidality. This dysfunction is associated with alterations in the polymorphisms of tryptophan hydroxylase gene expression, i.e., the rate-limiting enzyme which in turn modifies the biosynthesis of serotonin, contributing to the reduction of serotonergic activity. Since the prefrontal cortex and related structures play a major role in mood regulation, their participation in the pathophysiology of affective disorders and suicide is currently being discussed. A circuit integrated by prefrontal cortex, hippocampus, amygdaloid complex, lateral septal nucleus and other functionally related structures could be involved in the regulation of emotional memory, hedonism and decision-taking. The hippocampus is implicated in cognition and is one of the cerebral structures strongly affected by stress. Structural abnormalities in cortical and hippocampal areas and reduced hippocampal plasticity have been demonstrated in patients suffering from chronic stress and affective disorders. Reduced neurotrophin expression may be associated with structural abnormalities and reduced hippocampal plasticity. A decrease in the content of neurotrophins in the prefrontal cortex and hippocampus could be of relevance in suicidal behavior. Human post-mortem studies supported by living animals studies have demonstrated that antidepressants increase the activity of the brain-derived neurotrophic factor (BDNF) and increase the density of its receptor (BDNF-tyrosine kinase receptor B: trkB), which seems to participate in the therapeutic effects of drugs used in the treatment of depression. On the contrary, the reduction of BNDF trkB-receptor mRNA has been related to suicidal behavior, since a reduction of plasma BNDF levels has been reported in major depression. BNDF levels have also been suggested as a biological marker of suicidal depression. Abnormalities in the ventromedial prefrontal cortex in suicidal individuals largely correlate with the neurochemical deficits reported in this population. In fact, prefrontal hypofunction and impaired serotonergic responsivity are proportional to the lethality of the suicide attempt. Positron emission tomographic studies indicate lower ventromedial prefrontal cortex activity, behaviorally associated with high impulsivity, higher planning of suicidal intent, and higher-lethality suicide attempts. Other studies have also related structural abnormalities in amygdala with suicidality. The function of this region is critical regarding fear, anxiety, aggression and the recognition and response to danger, i.e., some behavioral patterns involved in suicidality. Anxiety commonly follows or precedes depression. Therefore, amygdaline dysfunction may increase the risk of suicidal behavior. For depressive-suicide attempters, the suicide act itself occurs at a moment of extreme anxiety, strongly suggesting amygdaloid complex participation in the process. Lastly, the lateral septal nucleus is related with anhedonia and hopelessness (despair). Since its neuronal firing rate increases after the experimental application of clinically effective antidepressant treatments. The septal nucleus is considered a target of these drugs, a suggestion supported by the observation that anhedonia is one of the main symptoms in depression and lateral septal nucleus activity is involved in hedonic process. Anhedonia, hopelessness and other depressive symptoms are significantly related to suicidal ideation. Taking into account that some patients with major depression are vulnerable to suicide, this vulnerability may result from the interaction of suicidality with environmental precipitants and a lowered threshold for suicidal behavior. Certainly, one of the psychiatric disorders associated with suicide is depression, which suggests a causal relationship and suggests the involvement of these brain structures in suicidality.<hr/>El suicidio es un fenómeno complejo y multifactorial. A pesar de que varios de los factores de riesgo ya han sido identificados, las bases neurobiológicas del suicidio no se han esclarecido del todo, aunque se han enfocado particularmente hacia la disfunción del sistema serotonérgico. Los primeros estudios indicaban que, en sujetos con intentos suicidas, se encuentran niveles reducidos del ácido 5-hidroxiindol-acético, principal metabolito de la serotonina, en el líquido cefalorraquídeo, independientemente del diagnóstico psiquiátrico previo. Más adelante, algunos estudios post-mortem han identificado alteraciones en los receptores presinápticos (5-HT1A) y postsinápticos (5-HT2A, 5-HT1A) de la corteza prefrontal ventromedial. Esta disfunción, al parecer, se asocia con alteraciones en los genes que codifican la expresión de enzimas implicadas en la síntesis y metabolismo de la serotonina, aunada a una alteración en la expresión genética de factores neurotróficos derivados del cerebro, los cuales intervienen en la regulación funcional de las neuronas serotonérgicas. En conjunto, estas alteraciones se han relacionado con la vulnerabilidad o la diátesis para el comportamiento suicida en individuos con predisposición a la conducta violenta e impulsiva o autoagresiva. Además, confluye una hiperactividad del eje hipotálamo-hipófisis-adrenal, confirmada por un incremento de la hormona adrenocorticotrófica y una reducción del número de receptores para esta hormona en la corteza prefrontal de suicidas. La corteza prefrontal desempeña un papel fundamental en la regulación del estado de ánimo y se le ha implicado tanto en la fisiopatología de los trastornos afectivos como en el suicidio. Por medio de estudios con tomografía por emisión de positrones, se determinó que en los sujetos con intento de suicidio existe una hipofuncionalidad de la corteza prefrontal ventromedial, lo cual se ha asociado con la impulsividad y la planeación para intentar suicidarse. Asimismo, el hipocampo se ha implicado en la cognición y es una estructura que participa en el estrés, un factor predisponente al suicidio. Algunos sistemas celulares también han sido implicados, por ejemplo, los factores de transcripción CREB (proteína ligada al AMP cíclico), los cuales están disminuidos en la corteza prefrontal, hipocampo y amígdala de suicidas. Algunos otros estudios sugieren incluso anormalidades estructurales en la amígdala. Aunque es especulativo proponer que la amígdala cumpla un papel específico en el suicidio, tal propuesta no carece de bases dado que esta región es crítica en la integración de la ansiedad y en la agresión, además de que guía las respuestas apropiadas que deben emitirse bajo situaciones de peligro. Por otro lado, el núcleo septal lateral se ha implicado en la desesperanza y en las acciones de diversos tratamientos antidepresivos. Entonces, se puede integrar un circuito anatómico y funcional en el cual participan como entrada los sistemas sensoriales, de ahí a estructuras integradoras de la memoria emocional, ubicadas principalmente en el lóbulo temporal, para de ahí pasar a estructuras de la neocorteza, principalmente la corteza prefrontal, mediante las proyecciones de núcleos talámicos. Esta vía integra la percepción del ambiente, información que es contrastada en los circuitos de la memoria emocional, para de ahí pasar a la toma de decisiones. Las alteraciones funcionales de este circuito, aunadas a factores ambientales adversos, parecen promover el acto suicida. En fin, en el suicidio participan estructuras cerebrales integradoras del estado afectivo, la memoria emocional, la impulsividad y la toma de decisiones. Quizá por todo ello, aunque se acepta la eficacia de los antidepresivos, del litio y de los antipsicóticos de segunda generación, se cuestiona aún la eficacia de los antipsicóticos convencionales, por su escasa acción en el estado afectivo. Aunque la depresión es una entidad clínica de riesgo para el suicidio, no es la única, pues también son factores de riesgo el trastorno bipolar y el trastorno esquizoafectivo. Cualquiera de ellos, aunado a agitación e impulsividad, debe llamar la atención para seleccionar el tratamiento farmacológico preventivo pertinente. <![CDATA[<b>Autoevaluación</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252008000400012&lng=es&nrm=iso&tlng=es Suicidal behavior is a complex and multifactorial phenomenon. At present, growing evidence shows the participation of biological traits in suicidality. Some findings suggest the dysfunction of the serotonin system, since serotonin and some of its receptor subtypes are involved in the modulation of such as affective behavior and cognition, among other behavioral processes. The content of 5-hydroxyindoleacetic acid, the major serotonin metabolite, is reduced in the cerebrospinal fluid of violent suicide attempters, independently of any other previous psychiatric diagnosis. In fact, this reduction may predict future suicide attempts and suicide completion. Post-mortem studies of ventromedial prefrontal cortex from suicide victims show decreased density of the 5-HT1A presynaptic serotonergic receptor subtype, and a compensatory upregulation of the 5-HT2A serotonergic post-synaptic receptor subtype. These observations on suicide strongly suggest a role of the two serotonin receptor subtypes located in this cortical brain region. Dysfunction of this region may support the diathesis concept (vulnerability) associated to suicidal behavior. In fact, some people display impulsive and self-aggressive behavior as part of their suicidality. This dysfunction is associated with alterations in the polymorphisms of tryptophan hydroxylase gene expression, i.e., the rate-limiting enzyme which in turn modifies the biosynthesis of serotonin, contributing to the reduction of serotonergic activity. Since the prefrontal cortex and related structures play a major role in mood regulation, their participation in the pathophysiology of affective disorders and suicide is currently being discussed. A circuit integrated by prefrontal cortex, hippocampus, amygdaloid complex, lateral septal nucleus and other functionally related structures could be involved in the regulation of emotional memory, hedonism and decision-taking. The hippocampus is implicated in cognition and is one of the cerebral structures strongly affected by stress. Structural abnormalities in cortical and hippocampal areas and reduced hippocampal plasticity have been demonstrated in patients suffering from chronic stress and affective disorders. Reduced neurotrophin expression may be associated with structural abnormalities and reduced hippocampal plasticity. A decrease in the content of neurotrophins in the prefrontal cortex and hippocampus could be of relevance in suicidal behavior. Human post-mortem studies supported by living animals studies have demonstrated that antidepressants increase the activity of the brain-derived neurotrophic factor (BDNF) and increase the density of its receptor (BDNF-tyrosine kinase receptor B: trkB), which seems to participate in the therapeutic effects of drugs used in the treatment of depression. On the contrary, the reduction of BNDF trkB-receptor mRNA has been related to suicidal behavior, since a reduction of plasma BNDF levels has been reported in major depression. BNDF levels have also been suggested as a biological marker of suicidal depression. Abnormalities in the ventromedial prefrontal cortex in suicidal individuals largely correlate with the neurochemical deficits reported in this population. In fact, prefrontal hypofunction and impaired serotonergic responsivity are proportional to the lethality of the suicide attempt. Positron emission tomographic studies indicate lower ventromedial prefrontal cortex activity, behaviorally associated with high impulsivity, higher planning of suicidal intent, and higher-lethality suicide attempts. Other studies have also related structural abnormalities in amygdala with suicidality. The function of this region is critical regarding fear, anxiety, aggression and the recognition and response to danger, i.e., some behavioral patterns involved in suicidality. Anxiety commonly follows or precedes depression. Therefore, amygdaline dysfunction may increase the risk of suicidal behavior. For depressive-suicide attempters, the suicide act itself occurs at a moment of extreme anxiety, strongly suggesting amygdaloid complex participation in the process. Lastly, the lateral septal nucleus is related with anhedonia and hopelessness (despair). Since its neuronal firing rate increases after the experimental application of clinically effective antidepressant treatments. The septal nucleus is considered a target of these drugs, a suggestion supported by the observation that anhedonia is one of the main symptoms in depression and lateral septal nucleus activity is involved in hedonic process. Anhedonia, hopelessness and other depressive symptoms are significantly related to suicidal ideation. Taking into account that some patients with major depression are vulnerable to suicide, this vulnerability may result from the interaction of suicidality with environmental precipitants and a lowered threshold for suicidal behavior. Certainly, one of the psychiatric disorders associated with suicide is depression, which suggests a causal relationship and suggests the involvement of these brain structures in suicidality.<hr/>El suicidio es un fenómeno complejo y multifactorial. A pesar de que varios de los factores de riesgo ya han sido identificados, las bases neurobiológicas del suicidio no se han esclarecido del todo, aunque se han enfocado particularmente hacia la disfunción del sistema serotonérgico. Los primeros estudios indicaban que, en sujetos con intentos suicidas, se encuentran niveles reducidos del ácido 5-hidroxiindol-acético, principal metabolito de la serotonina, en el líquido cefalorraquídeo, independientemente del diagnóstico psiquiátrico previo. Más adelante, algunos estudios post-mortem han identificado alteraciones en los receptores presinápticos (5-HT1A) y postsinápticos (5-HT2A, 5-HT1A) de la corteza prefrontal ventromedial. Esta disfunción, al parecer, se asocia con alteraciones en los genes que codifican la expresión de enzimas implicadas en la síntesis y metabolismo de la serotonina, aunada a una alteración en la expresión genética de factores neurotróficos derivados del cerebro, los cuales intervienen en la regulación funcional de las neuronas serotonérgicas. En conjunto, estas alteraciones se han relacionado con la vulnerabilidad o la diátesis para el comportamiento suicida en individuos con predisposición a la conducta violenta e impulsiva o autoagresiva. Además, confluye una hiperactividad del eje hipotálamo-hipófisis-adrenal, confirmada por un incremento de la hormona adrenocorticotrófica y una reducción del número de receptores para esta hormona en la corteza prefrontal de suicidas. La corteza prefrontal desempeña un papel fundamental en la regulación del estado de ánimo y se le ha implicado tanto en la fisiopatología de los trastornos afectivos como en el suicidio. Por medio de estudios con tomografía por emisión de positrones, se determinó que en los sujetos con intento de suicidio existe una hipofuncionalidad de la corteza prefrontal ventromedial, lo cual se ha asociado con la impulsividad y la planeación para intentar suicidarse. Asimismo, el hipocampo se ha implicado en la cognición y es una estructura que participa en el estrés, un factor predisponente al suicidio. Algunos sistemas celulares también han sido implicados, por ejemplo, los factores de transcripción CREB (proteína ligada al AMP cíclico), los cuales están disminuidos en la corteza prefrontal, hipocampo y amígdala de suicidas. Algunos otros estudios sugieren incluso anormalidades estructurales en la amígdala. Aunque es especulativo proponer que la amígdala cumpla un papel específico en el suicidio, tal propuesta no carece de bases dado que esta región es crítica en la integración de la ansiedad y en la agresión, además de que guía las respuestas apropiadas que deben emitirse bajo situaciones de peligro. Por otro lado, el núcleo septal lateral se ha implicado en la desesperanza y en las acciones de diversos tratamientos antidepresivos. Entonces, se puede integrar un circuito anatómico y funcional en el cual participan como entrada los sistemas sensoriales, de ahí a estructuras integradoras de la memoria emocional, ubicadas principalmente en el lóbulo temporal, para de ahí pasar a estructuras de la neocorteza, principalmente la corteza prefrontal, mediante las proyecciones de núcleos talámicos. Esta vía integra la percepción del ambiente, información que es contrastada en los circuitos de la memoria emocional, para de ahí pasar a la toma de decisiones. Las alteraciones funcionales de este circuito, aunadas a factores ambientales adversos, parecen promover el acto suicida. En fin, en el suicidio participan estructuras cerebrales integradoras del estado afectivo, la memoria emocional, la impulsividad y la toma de decisiones. Quizá por todo ello, aunque se acepta la eficacia de los antidepresivos, del litio y de los antipsicóticos de segunda generación, se cuestiona aún la eficacia de los antipsicóticos convencionales, por su escasa acción en el estado afectivo. Aunque la depresión es una entidad clínica de riesgo para el suicidio, no es la única, pues también son factores de riesgo el trastorno bipolar y el trastorno esquizoafectivo. Cualquiera de ellos, aunado a agitación e impulsividad, debe llamar la atención para seleccionar el tratamiento farmacológico preventivo pertinente.