Scielo RSS <![CDATA[Salud mental]]> http://www.scielo.org.mx/rss.php?pid=0185-332520100006&lang=pt vol. 33 num. 6 lang. pt <![CDATA[SciELO Logo]]> http://www.scielo.org.mx/img/en/fbpelogp.gif http://www.scielo.org.mx <![CDATA[<b>The Castañeda's contribution to the professionalization of Mexican psychiatry, 1910-1968</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600001&lng=pt&nrm=iso&tlng=pt On September 1, 1910, more than two thousand people celebrated the one hundredth anniversary of Mexico's Proclamation of Independence with the inauguration of a psychiatric hospital. According to the event's official chronicler, the 25 buildings constructed by order of president Porfirio Díaz on the site of the former Castañeda Hacienda would place Mexico among the leading countries in the world in treating mental health pathologies. But, what had been Mexico's development in this field during the XIX century? Could we consider La Castañeda <<the birthplace of public psychiatry&gt;&gt; in Mexico? This work analyzes La Castañeda's contribution to the professionalization of psychiatry in Mexico, not only by looking at the place that research and teaching traditionally had in hospitals, but also by looking at other mechanisms that help to form a discipline, such as the capacity to bring light to scientific societies and to bring credibility to a new medical field such as psychiatry, so much in need of therapeutic successes in those years. In the XIX century around 400 articles, theses and books by Mexican, Hispanic and foreign authors were published that dealt with topics associated with psychiatry. The old hospitals of the colonial system such as San Hipólito and La Canoa established a form of treatment called <<moral treatment&gt;&gt;, precursor to psychiatry, and were directed by a doctor substituting a director-administrator. Between 1865-1910, five projects for a modern mental hospital were made, one of which saw fruition in the form of La Castañeda. In 1887 the first course dealing with mental illness was taught and in 1906 the first specialization in psychiatry was brought about. Nonetheless, this movement was cut short by the Revolution of 1910 which assailed the country for almost a decade and provoked that La Castañeda be left without state support. The professionalization of Mexican psychiatry can be divided in three stages: 1910-1925, a period marked by the decomposition brought on by the war; 1925-1945, characterized by the major medical and administrative reform of the hospital, and 1945-1968, a stage which included the slow dismantling of La Castañeda. In the first stage, La Castañeda saw a certain level of deterioration in its assistance practices, as 25% of patients who entered between 1914-1916 were not diagnosed, and 45% of patients of those entering between 1917-1920 were not diagnosed either. This fact is explained by the institution's instability in those years. Between 1910-1923, La Castañeda had twelve directors. Academic courses in mental illness continued to be offered and a medical society was formed, but with few results. In 1925 Public Welfare asked doctor Enrique Aragón to inspect the Asylum and present a detailed report of any reforms needed. The three most serious problems he discovered were: the deficient way in which doctors handled patient's clinical records, shortages and poor training of personnel and the fact that there was almost no research being done. From 1925-1945, La Castañeda experienced great reforms thanks to three doctors who wanted to professionalize psychiatry in Mexico and place it at a competitive level with hospitals around the world, which they had seen in visits to Europe and the U.S. These doctors were Samuel Ramírez Moreno, Alfonso Millán Maldonado and Manuel Guevara Oropeza, who received support from the federal government. In 1929 a system of occupational therapy was established as a means of rehabilitation, and outpatient services were offered to those not needing hospitalization. In 1932 a Children's Ward was inaugurated and the following year the School for Abnormal Children, both directed by Mathilde Rodríguez Cabo, the first woman psychiatrist in Mexico. Alongside Ramírez Moreno, she began a project offering courses in psychiatric nursing and caregiving. In 1935 the Drug Addicts Unit was inaugurated, and in the years following shock therapies were introduced. A laboratory was established to perform traditional clinical analyses, as well as bacteriological and pathological analyses, and microphotography, both to improve diagnoses and to move research forward. All was influenced to a great extent by Spanish neurobiology which came about after the Spanish Civil War, when exiles such as Dionisio Nieto were received in Mexico. In order to strengthen the guild, at this stage there were important initiatives. In 1934, the Revista Mexicana de Psiquiatría, Neurología y Medicina Legal, the first journal in its field in Mexico, was published. In 1937 the Sociedad Mexicana de Neurología y Psiquiatría was founded, as well as its official organ, Archivos de Neurología y Psiquiatría de México. Around 1943, a project which would become Mexico's policy of mental health for the years 1945-1968 began to be conceived. This policy would lead to the demolition of La Castañeda, and replace it with farms or field homes for the mentally ill. This therapeutic model, with chronic patients in mind, was based on recreational and occupational therapies, and its intention was to place patients in contact with nature, under a regimen of liberty and dedicated to productive and dignified activities. Ye t these farms were located far from urban centers, isolating patients even further from family. In fact, psychiatry itself was also isolated from the rest of the medical world. La Castañeda closed on June 29, 1968, and with it more than 68 000 lives, could they talk today, might well tell this story differently.<hr/>El 1 de septiembre de 1910 más de dos mil personas conmemoraron el Centenario de la Proclamación de la Independencia de México con la inauguración de un manicomio. Según la opinión del cronista oficial de los festejos, los 25 edificios que mandó a construir el presidente Porfirio Díaz en la antigua hacienda de La Castañeda pondrían a México a la altura de los países más avanzados en el tratamiento de las enfermedades mentales. Pero ¿qué desarrollo había tenido en México este campo durante el siglo XIX? ¿Podemos considerar a La Castañeda como <<la cuna de la psiquiatría pública&gt;&gt; mexicana? En este trabajo se analiza la contribución de La Castañeda a la profesionalización de la psiquiatría mexicana mediante el lugar que tradicionalmente le han dado los hospitales a la enseñanza y la investigación, pero también a través de otros mecanismos que forjan una disciplina, como la capacidad para alumbrar en su seno sociedades científicas y para dotar de credibilidad a un nuevo campo médico tan necesitado de éxitos terapéuticos, como lo fue la psiquiatría en esos años. Durante el siglo XIX se publicaron alrededor de 400 títulos de tema psiquiátrico entre artículos, tesis y libros de autores mexicanos e hispanos, así como traducciones de autores extranjeros. Por otro lado, los viejos hospitales coloniales como San Hipólito y La Canoa establecieron el tratamiento moral, la terapéutica con la que nació la psiquiatría, y fueron dirigidos por un médico en sustitución del director-administrador. Entre 1865 y 1910 se elaboraron cinco proyectos de <<manicomio moderno&gt;&gt;, uno de los cuales culminó finalmente en La Castañeda; en 1887 se impartió por primera vez la cátedra de enfermedades mentales y en 1906 se estableció la especialidad en psiquiatría. Sin embargo, esta gran vitalidad fue atropellada por la contienda revolucionaria que asoló al país durante casi una década y provocó que el Manicomio creciera sin el apoyo del Estado, de un Estado fuerte que sucumbió muy pronto cuando en mayo de 1911 Porfirio Díaz tomó el camino del exilio. La profesionalización de la psiquiatría mexicana se puede dividir en tres etapas. La primera, de 1910 a 1925, se caracterizó por un relajamiento de sus prácticas asistenciales a causa de la inestabilidad institucional que vivió el Manicomio. La segunda, de 1925 a 1945, conoció la mayor reforma médica y administrativa que permitió instaurar a gran escala la terapia ocupacional como un medio de rehabilitación, se empezó a dar consulta externa a pacientes que no necesitaran hospitalización, se inauguró el Pabellón Infantil, la Escuela para Niños Anormales y el Pabellón de Toxicómanos, se impartieron clases de enfermería psiquiátrica, se publicó la primera revista de la especialidad y se fundó la Sociedad Mexicana de Neurología y Psiquiatría. Hacia 1943 comenzó a idearse el proyecto que se convertiría en la política de salud mental del Estado mexicano entre 1945 y 1968, la tercera etapa, y que llevaría al lento desmantelamiento de La Castañeda hasta su demolición: las Granjas para enfermos mentales. El Manicomio se cerró el 29 de junio de 1968 y con él más de 68 000 vidas que, si hablaran, contarían esta historia de otra manera. <![CDATA[<b>Cognitive function evaluation</b>: <b>attention and memory in panic disorder patients</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600002&lng=pt&nrm=iso&tlng=pt Evidence from recent studies about the epidemiology of panic disorder (PD) indicates that it is present in 4.7% of general population. In Mexico City, 2.9% of females and 1.9% of males are affected by this disease. Due to the incidence cited above, it is considered an important mental health problem that has impacted social, labor and familiar areas. On the other hand, PD is frequently present in comorbidity with other disorders like major depression, social phobia and generalized anxiety disorder. Moreover, in some cases, it may lead to a suicide risk. PD is characterized by recurrent, unexpected panic attacks, and is commonly associated with agoraphobia. A panic attack is defined as a discrete period of fear or discomfort that includes physical, cognitive and behavioral symptoms. Physical symptoms comprise short breath, palpitations, sweating, dizziness, gastrointestinal discomfort, and chest pain. Cognitive symptoms are associated with catastrophic interpretation of bodily sensations; behavioral symptoms are mainly avoidant of different places, situations and actions that patient had associated with fear of loss of control. In the past few years there has been a growing interest in the neuropsychology of anxiety disorders. Neuropsychological evaluation is relevant because it implies an objective assessment of the cognitive and behavioral abilities and weaknesses that make possible the prediction of the course of the disorder and the effects of treatment modalities. One of the most important contributions of neuropsychological evaluation is the identification of stable patterns of cognitive profiles of a specific disorder considered as neurocognitive endophenotypes. Some recent studies have demonstrated the relationship between neuropsychological alterations and anxiety; nevertheless, most of them were observed in obsessive-compulsive disorder patients. On the other hand, studies examining neuropsychological functioning in PD patients are scarce and report conflicting results. The main objective of the present study was to evaluate whether PD patients with and without agoraphobia, who attended the National Institute of Psychiatry <<Ramón de la Fuente&gt;&gt; in Mexico City, showed neuropsychological impairments relative to healthy controls in attention, memory and executive functions. We studied a total sample of 48 subjects (24 patients with PD, the patients sample was selected according to a psychiatric evaluation, based on DSM-IV-TR criteria. Inclusion criteria were age between 19 and 56, men or women, without previous pharmacological or psychotherapeutically treatment; and 24 gender, age and education matched healthy control subjects). A neuropsychological test battery (Neuropsi Attention and Memory) in Spanish with norms by age and educational level was administered. The Neuropsi assesses orientation, attention and concentration, executive functions, working memory and immediate and delayed verbal and visual memory. Likewise, all patients were assessed with the Anxiety Sensitivity Index, Beck's Anxiety Inventory and Panic Disorder Severity Scale. According to this psychometric evaluation, the PD patients showed severe anxiety, high anxiety sensitivity, as well as a severe degree of panic symptoms. The differences between PD patients and control subjects in neuropsychological performance were determined through one way analysis of variance (p<0.05) with the assistance of the SPSS 12. The results of the present study indicate that the neuropsychological test performance of patients with PD is diminished relative to that of the health control. According to obtained results, there were significant differences in the total score of executive functions and attention, memory and global attention and memory between patients and healthy controls. In the analysis of different subscales, it was found that patients had reduced performance in visual search, digit backward span, world list free recall, Rey-Ostereith Complex Figure Test encoding and retrieval, word list cued recall, faces retrieval and in diverse executive functions like category formation test, semantic and phonological verbal fluency, as well as design fluency. This suggests that PD is associated with alterations in tasks that require flexibility in the mental processes, short-term memory, working memory, and in the generation of strategies to solve problems. However, it is possible that these alterations were present before the onset of panic disorder and predispose the ulterior development of this disorder. In the visual detection subscale, that evaluates selective attention, there were also differences in latency of response because patients were slower than healthy controls trying to find the correct figure. This deficiency is associated with the difficulty of PD patients to perceive important details of the environment due to the extreme attention in the corporal sensations. Besides, no group differences were found in orientation, attention and concentration. These findings are consistent with previous studies with PD patients, where impairments in verbal memory, executive functions and visuospatial memory were found. Nevertheless, these findings differ from the reported by others studies, where neuropsychological alterations in PD patients were found. These discrepancies could be due to methodological procedures in the sample selection, pharmacological treatment, intensity of anxiety, and the use of different neuropsychological instruments. In the present study, the clinical sample was characterized by absence of pharmacological and psychotherapeutic treatments before neuropsychological evaluation was done with the Neuropsi. A notable finding was that, in the face recognition subscale, patients had better scores than controls. This can be related to a previous reported finding, which suggested that PD patients pay more attention to the details of a face to evaluate if these are safe or unsafe before the possibility of having a panic attack. Also, it is possible to consider it like an special ability developed by these patients as a compensatory behavior before the disability caused by this disorder and the vulnerability they experience when not having control of their symptoms. In conclusion, we have demonstrated deficits in the visuospatial and verbal memory, and executive functions in PD patients. This finding supported a disturbance in the amygdaline fronto-temporal neural network in the disorder, related in the conditioned fear network involved in the etiology of panic disorder. Future neuropsychological studies will benefit from use of neuroimaging studies to examine pattern of brain activation and elucidate the pathophysiology features of the disorder. As well as determine whether cognitive performance varies as a function of severity of panic symptoms.<hr/>De acuerdo a Kessler, el 4.7% de la población general presenta Trastorno de Pánico (TP) a lo largo de la vida, específicamente en la Ciudad de México el TP tiene una prevalencia en la vida de 1.1% en los hombres y de 2.5% en las mujeres, por lo que se considera un problema de gran relevancia. Aunado a esto, uno de los grandes problemas de este padecimiento es el alto índice de comorbilidad que presenta con otros trastornos psiquiátricos como la depresión mayor, la fobia social, el trastorno por ansiedad generalizada y el abuso de sustancias. De acuerdo con el DSM-IV-TR, el TP se caracteriza por la aparición de crisis de angustia inesperadas y recurrentes, inquietud persistente por la posibilidad de tener más crisis, preocupación por las implicaciones de las mismas o sus consecuencias y/o un cambio significativo del comportamiento relacionado con ellas. La evaluación neuropsicológica es relevante, ya que a través de ésta es posible obtener una valoración objetiva que permite conocer las habilidades y déficits cognoscitivos y conductuales de los pacientes con trastornos psiquiátricos para hacer una predicción sobre el curso de la enfermedad, elegir el tipo de tratamiento de forma objetiva, identificar patrones estables de déficits neuropsicológicos así como establecer estrategias que mejoren el pronóstico del trastorno. Diversos estudios han demostrado recientemente la relación entre algunas alteraciones neuropsicológicas y la ansiedad; sin embargo, la mayoría de éstos se han centrado en el trastorno obsesivo-compulsivo. Aunado a esto, los resultados encontrados en investigaciones que han evaluado las funciones cognitivas en el TP, no han sido consistentes. El objetivo del presente estudio fue determinar si existen déficits neuropsicológicos en pacientes diagnosticados con TP con o sin agorafobia que acudieron al servicio de preconsulta del Instituto Nacional de Psiquiatría Ramón de la Fuente, en comparación con sujetos control en los dominios de atención, memoria y funciones ejecutivas. Se seleccionaron dos grupos: uno de 24 sujetos diagnosticados con TP, de acuerdo al DSM-IV-TR, sin tratamiento farmacológico y/o psicoterapéutico previo; y otro de 24 sujetos sanos comparados formando pares por sexo, edad y escolaridad con el primero. Se les aplicó una batería neuropsicológica (Neuropsi Atención y Memoria) que evalúa orientación, atención y concentración, memoria de trabajo, memoria verbal y visual, y funciones ejecutivas y motoras. El Neuropsi Atención y Memoria cuenta con normas obtenidas en la población mexicana, considerando la edad y la escolaridad. Las diferencias en el desempeño cognitivo entre el grupo control y el grupo con TP fueron analizadas por medio de un Análisis de Varianza (con p<0.05). Los resultados mostraron que los sujetos con TP puntuaron significativamente más bajo que los controles en el puntaje total de atención y memoria, en el puntaje del total de atención y funciones ejecutivas, y el total de memoria. El análisis de las subpruebas específicas reveló déficits en la memoria verbal, la memoria visoespacial inmediata y la evocada, y en diversas funciones ejecutivas: formación de categorías, fluidez verbal semántica y fonológica, y fluidez no verbal. Los hallazgos encontrados en este estudio apoyan la noción de que la ansiedad (específicamente el TP) afecta la memoria verbal y la visoespacial así como las funciones ejecutivas. Los pacientes con TP mostraron alteraciones significativas en tareas que requieren de la capacidad de cambiar de foco de atención, flexibilidad en los procesos cognitivos, capacidad de inhibir respuestas inadecuadas, memoria a corto plazo y memoria de trabajo. <![CDATA[<b>Assertiveness levels, sociodemographic profile, nicotine dependence and reasons for smoking in a group of smokers attending teatment to stop smoking</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600003&lng=pt&nrm=iso&tlng=pt Introduction Tobacco consumption is a serious public health problem and the principal cause of death worldwide. It is linked to chronic obstructive pulmonary disease (COPD), coronary disease, and various cancers such as lung cancer, which is the most frequent, and cancer of the larynx and other organs. Smoking affects the quality of life of millions of people. Those who live with smokers also become involuntary or passive smokers. It is important to determine the factors that influence initiation and continuation of smoking and the reasons that facilitate or favor smoking cessation. The dependence of cigarette smoking acts as a modulator of the relationship that smokers have with their social environment and on the expression of their feelings. We considered important to study the assertiveness of smokers, which is considered to be the social skill that individuals have to express what they think, feel and opine about respecting their rights and the rights of others as a factor that may influence smoking cessation or continuation of smoking. Objective We undertook this study to determine the levels of assertiveness and the sociodemographic profile of a population of 130 patients who were smokers and who came to the <<Clinic against Smoking&gt;&gt; located at a tertiary level teaching and research hospital in Mexico City. This was the first attempt for these patients to undergo cognitive behavioral treatment to stop smoking. We sought to determine if there are any significant differences between those patients who smoke and who continue treatment and those patients who abandon treatment. Material and methods Only patients who were active smokers were studied. Of a total of 130 subjects, 65 completed the treatment and 65 abandoned treatment. For each patient, the socioeconomic profile was investigated with regard to gender, age, marital status, education, occupation, and contribution to the family income. The Gambrill and Richey Assertiveness Inventory for the Mexico City population was used. The Fagerström questionnaire was applied for evaluation of nicotine dependence, with a value &gt;6 considered to be positive to qualify as dependence and the Russell reasons for smoking, which include stress reduction, the need to smoke, relaxation, the stimuli to perform activities and manipulation. Results were analyzed by descriptive analysis evaluating the assertiveness profile by probability of assertive response and the degree of discomfort classified as high, medium and low. The level of assertiveness was diagnosed according to the probability of response and the degree of discomfort as indifferent, assertive, nonassertive, average level of assertiveness and anxiety; a group was not classified between the groups mentioned. We used Χ2 for comparison of the levels of assertiveness between those who completed the treatment and those who did not. Results Of the 130 subjects studied, 65 completed the study satisfactorily and 65 abandoned treatment. Average age of the group of patients was 39.8 years (range: 19-60 years). There were 56.9% (74/130) females and 43.07% (56/130) males. It was determined that 60% of the population lived with a partner (78/130). Of the study population, those reporting a higher educational level (51.5%) (67/130) had a slight predominance over those subjects with either primary or secondary level of education. Of the 130 patients studied with the Fagerström questionnaire, 56.4% were nicotine dependent (73/130) and 47.4% (57/130) were not dependent. According to the Russell questionnaire for reasons for smoking, the most important reasons for smoking were stress reduction in 30.4% (42/130), the need to smoke in 33.1% (43/130) and for relaxation, with no difference between those who completed treatment and those who abandoned treatment. Stimulation, habit and manipulation were less frequently observed reasons. In general, the population studied presented a low level of assertiveness and a deficit in social behavior without significant differences between those who leave or continue the treatment. Only 20% of all smokers were assertive, 19% were not assertive, 30% were indifferent, 15% had an average level of assertiveness, 5% demonstrated anxiety and 36% of those who had other levels remained in the <<unclassified&gt;&gt; group. The analysis of reactives demonstrated that the smokers presented a low probability of response in the areas that manifested in the expression of annoyance, anger or disagreement with others, recognizing personal limitations and acting in defense of rights in commercial situations and interactions with neighbors. They demonstrated a greater degree of discomfort in the areas of confrontation, defense of views and resisting pressure from others. Discussion Knowledge of the socioeconomic environment of smokers who desire to stop smoking using cognitive behavioral therapy is important because the environment in which the smoker lives exerts an influence on the success or failure of the attempt to stop smoking. Gender, age, living with a partner, economic status and educational level are factors that may influence adherence to treatment and also influence the tendency to abandon treatment. Nicotine dependence was a determinant factor regarding completion or abandonment of treatment. Stress reduction and searching for and needing relaxation were the most frequently mentioned reasons for smoking. The level of assertiveness does not appear to playa definitive role for treatment success or for abandoning the smoking habit. Only 20% of the smokers were assertive and, of those, only half completed the treatment, with no difference between those who did not complete the treatment. The probability of an assertive response and the degree of discomfort did not show differences in the two groups mentioned, which suggests that assertiveness does not have a great influence on the final results. In general, the population studied had a deficit in social abilities. In the reactive analysis it was found that there is an opposition in the areas of defense of opinions and for resisting pressure from others, for manifesting annoyance, anger or disagreement and in regard to the defense of rights in commercial situations and interaction with others. There were no significant differences observed in between-group comparisons (Χ2 0.406). There were also no significant differences between those who are assertive and those who have a low level of assertiveness. These individuals prefer to reduce stress, satisfy their needs and seek relaxation or the stimulation produced by nicotine vs. the effort required to follow smoking cessation treatment, particularly within a social environment where smoking may be an element that eases relationships with others. The observations obtained in this study suggest that assertiveness training specific to the type of smoker who tends to abandon treatment may be appropriate to obtain positive results and contribute not only to avoid abandoning treatment but also to maintaining positive results and to avoid relapses. This training may influence those susceptible subjects to avoid initiating a smoking habit. Conclusion The level of assertiveness is not an important factor to explain the success or failure of a smoking cessation program. Training in assertiveness may be useful to enhance success of treatment to quit smoking.<hr/>Introducción El tabaquismo es un problema de salud pública, es la principal causa de muerte evitable en el mundo, se vincula a padecimientos -como enfermedad pulmonar obstructiva crónica (EPOC), enfermedad coronaria y diversos cánceres, como el de pulmón, que es el más frecuente, y el de laringe- y afecta la calidad de vida de miles de seres. Los que conviven con el fumador se convierten en <<fumadores involuntarios&gt;&gt; o pasivos. Es importante conocer los factores que influyen en el inicio y mantenimiento de la conducta de fumar y los motivos para abandonarla. El hábito de fumar cigarrillos actúa como modulador de la relación entre el fumador y el medio social en que se desenvuelve y en la expresión de sus propios sentimientos. Se consideró importante estudiar la asertividad como la habilidad social para comportarse y expresar lo que piensa, siente y opina el fumador respetando sus derechos y los de los demás como un factor que puede influir en la cesación del consumo de tabaco. Objetivo Conocer la influencia de los niveles de asertividad y el perfil sociodemográfico de una población de 130 pacientes fumadores que acudieron por primera vez a tratamiento cognitivo-conductual para dejar de fumar, a la Clínica Contra el Tabaquismo de un hospital de tercer nivel con instalaciones de enseñanza e investigación, para determinar si existen diferencias entre los que siguen el tratamiento y los que lo abandonan. Material y métodos Con una investigación descriptiva transversal, se estudiaron sólo pacientes fumadores activos. En cada paciente se investigó el perfil socioeconómico para obtener información de género, edad, convivencia con una pareja, grado de escolaridad y ocupación. Se empleó el Inventario de Asertividad de Gambrill y Richey estandarizado para la población de la Ciudad de México. Se aplicaron los cuestionarios de Frageström para valorar la dependencia a la nicotina y el de motivos de fumar de Russell que comprende reducir tensión, necesidad, relajamiento, estímulo para reducir actividades y manipulación. Los resultados se analizaron por estadística descriptiva y se hizo una comparación por Χ² de los niveles de asertividad que presentaron los que terminaron el tratamiento y los que lo interrumpieron. Resultados Del total de 130, terminaron el tratamiento 65 y lo abandonó el mismo número. La población estudiada presentó un bajo nivel de asertividad y un déficit en habilidades sociales. El análisis de reactivos demostró que los fumadores presentan un mayor grado de incomodidad (GI) en las áreas de confrontación, defensa de opiniones y resistencia a la presión de otras personas y una baja probabilidad de respuesta (PR) en las áreas de manifestar molestia, enfado o desacuerdo, reconocer limitaciones personales y en la defensa de derechos en situaciones comerciales e interacciones con personas cercanas. Las circunstancias observadas sugieren que es conveniente un entrenamiento asertivo específico para esta población de fumadores. Discusión El conocimiento del estado socioeconómico de los fumadores que se someten a un tratamiento cognitivo-conductual para dejar de fumar es importante porque el medio influye en la adherencia o el abandono del intento para dejar el tabaco. El género, la edad, la pareja y el nivel educacional influyen en la adherencia al tratamiento o en su abandono. La dependencia a la nicotina puede ser un factor importante. La reducción de la tensión y la necesidad de relajación fueron las razones más frecuentemente encontradas para continuar fumando. El nivel de asertividad no parece cumplir un papel importante para el éxito o abandono del tratamiento para dejar de fumar. Sólo 20% de los fumadores resultaron asertivos y de éstos sólo la mitad completó el tratamiento sin diferencias con los que sí lo terminaron. La probabilidad de una repuesta asertiva y el grado de incomodidad no tuvieron diferencias entre los dos grupos, lo que sugiere que la asertividad no cumple un papel importante en los resultados finales. En general, la población estudiada mostró un déficit de habilidades sociales. En el análisis de reactivos la oposición en las áreas de defensa de opiniones y de resistencia a la presión de otros para manifestar incomodidad, angustia o desagrado en relación con la defensa de derechos en situaciones comerciales fueron importantes sin diferencias significativas (Χ² = 0.406). Tampoco hay diferencias ente los asertivos y los de baja asertividad; estos últimos prefieren continuar fumando con una sensación de relajamiento o estimulación producidos por la nicotina a la tensión que implica dejar de fumar, particularmente en un medio donde el fumar facilita la relación con los demás. Es posible que un entrenamiento asertivo pueda mejorar los resultados no sólo para terminar un tratamiento sino para evitar recaídas. Este tratamiento serviría también para impedir el inicio del consumo de tabaco. Conclusión La asertividad no influye en la adherencia o abandono de un tratamiento para dejar de fumar. Un entrenamiento asertivo específico simultáneo con la terapia grupal sería útil para apoyar la adherencia al tratamiento de la dependencia a la nicotina en un determinado medio social. <![CDATA[<b>Gender inequities, substance abuse and treatment barriers in women in prison</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600004&lng=pt&nrm=iso&tlng=pt The vast majority of women in Mexican prisons have several mental health disorders and addictions, as well as problems obtaining access to treatment for this type of problems. These women's personal background and prison conditions reflect the unresolved problems of the country, such as education and illiteracy, access to health and housing and inequity in the justice systems. The literature has shown that substance abuse affects female prisoners to a greater extent than other women, and that their disadvantaged socio-economic status makes them more likely to engage in and continue substance abuse. Other aspects that exacerbate this vulnerability are their low educational attainment, lack of job skills, and exposure to stigmatization and discrimination in addition to the physical and psychological consequences of addictive behavior. One aspect that has been internationally acknowledged is that gender inequities make women's health more vulnerable, particularly that of female prisoners, since they have greater health deficits and more treatment barriers. International literature has shown that female users of psychoactive substances in general face more barriers than men in seeking or continuing treatment. Research has also shown that the most common personal barriers in women are denial, shame and guilt. Likewise, women's anxiety and depressive disorders tend to be more prevalent and severe, which in turn prevents them from seeking help when they have substance abuse problems. The most common family-related barriers are the difficulty of attending treatment due to family, partner or childcare obligations, pregnancy or fear of losing custody of their children. The main barriers faced by women regarding treatment institutions are the insensitivity or inadequate training of the staff that work there, prejudice and negative attitudes towards women, lack of information on available treatment and extremely long waiting lists. As a result of the above, the aim of this study is to document the barriers to the treatment of addictions of female prisoners, a disadvantaged group that has rarely been studied in Mexico, in order to understand certain aspects related to this population's access to treatment and continuation of the latter. The design used for this research is an ex post facto, descriptive, non-experimental, cross-sectional field study. The sample consisted of 213 women, chosen for convenience, who met the following criteria: alcohol and drug users, ages 18 to 65, able to read and write and with no psychiatric disorders or handicaps that would prevent the interview. The women that participated in this study were drawn from two Mexico City prisons: the Centro Preventivo Femenil Oriente, which houses women that have been accused, tried and sentenced, and the Centro de Readaptación Social Femenil Tepepan, where the inmates are women who have been sentenced and also have psychiatric problems. The ethical care observed included informing the interviewees of the objectives of the study, voluntary participation, confidential handling of the information and the use of witnesses, as well as guaranteeing participants the right to abandon the study and not to answer questions they found uncomfortable. The instrument was designed as a semi-structured interview with 242 questions covering various areas including Allen's Questionnaire on Treatment Barriers. It can be self-administered by the respondents, has internal consistency, construct and content validity and was adapted by Romero (2002). Some of the respondents had to have the questionnaire read out to them because of their low educational attainment. This questionnaire consists of 41 items, 30 of which are divided into three categories: 1. characteristics of treatment services, 2. beliefs, feelings or thoughts, and 3. socio-environmental aspects. Each category also includes an open question to discover other types of barriers not included in the three categories. The results yielded the following socio-demographic profile of the interviewees: 45.5% were in the 28 to 40 year age group; and had had 6 or less years' education (41.3%) or completed junior high school (36.2%). The majority were single (48.6%) or common law (21.6%), while 50.7% had children under the age of 18. Certain other characteristics of this sample such as depression, violence and alcohol and drug use have been reported in other studies. Of the total group of women that had received treatment at some time in their lives, 52.6% (n = 112) mentioned some type of barrier to treatment for addictions. A total of 29.1% (n = 62) of these women mentioned some type of barrier to treatment for alcohol use, while 44.1 % (n = 94) cited some type of barrier to treatment for drug use. Lastly, 39.2% (n = 44) mentioned some type of barrier to treatment for both types of consumption. An analysis of the treatment sub-scale by socio-demographic variable showed greater difficulty in obtaining treatment among women ages 28 to 40 and among those with children under 18. Statistically significant differences were observed regarding the type of offense (robbery) and availability of treatment. As for the beliefs, feelings and thoughts sub-scale, statistically significant differences were found among women with children under 18 and those finding it hard to abandon consumption. The sub-scale related to situational aspects, such as rejection from friends, proved to be the main barrier to enter treatment and was statistically significant among single women. The results of this study pose challenges to the health and mental health service sector regarding the timely treatment and rehabilitation of marginalized women. Likewise, acknowledging gender inequities is crucial when it comes to designing health promotion strategies. Without this perspective, their effectiveness could be jeopardized and gender inequalities actually exacerbated.<hr/>La gran mayoría de las mujeres recluidas en las prisiones de México presentan una gran cantidad de trastornos de salud mental y adicciones, así como dificultades para acceder al tratamiento para este tipo de problemas. Los antecedentes personales y las condiciones de reclusión de estas mujeres reflejan los problemas no resueltos del país como son educación y analfabetismo, acceso a la salud, vivienda e inequidad en los sistemas de procuración de justicia. En la bibliografía se ha señalado que el abuso de sustancias afecta a las mujeres presas en mayor medida que a otras mujeres y que su situación socioeconómica desfavorable las hace más susceptibles de incidir y prevalecer en la conducta de abuso de sustancias. Otros aspectos que acentúan esta vulnerabilidad son el bajo nivel educativo, las pocas habilidades para el trabajo, la exposición a la estigmatización y la discriminación, además de las consecuencias físicas y psicológicas de la conducta adictiva. Un aspecto reconocido internacionalmente es que las inequidades de género vulneran de manera particular la salud de las mujeres, lo cual es aún más evidente en las mujeres presas, pues presentan mayores déficits en su salud y mayor número de barreras al tratamiento. Se ha documentado en la bibliografía internacional que las usuarias de sustancias psicoactivas en general se enfrentan a un mayor número de barreras que los hombres para buscar o seguir un tratamiento. Por lo anterior, el objetivo del estudio es documentar las barreras al tratamiento de adicciones de mujeres en prisión, una población desfavorecida poco estudiada en México a fin de entender algunos aspectos relacionados con el acceso a tratamientos de esta población y su permanencia en ellos. El diseño utilizado para esta investigación corresponde a un estudio de campo transversal no experimental, descriptivo, ex post facto. La muestra se conformó de 213 mujeres, seleccionadas por conveniencia, con los siguientes criterios: usuarias de alcohol y drogas, edad de 1 8 a 65 años, que supieran leer y escribir, sin trastorno psiquiátrico o discapacidad que impidiera la entrevista. Las mujeres que participaron en este estudio se seleccionaron de dos prisiones de la Ciudad de México: el Centro Preventivo Femenil Oriente, donde se encuentran mujeres indiciadas, procesadas y sentenciadas, y el Centro de Readaptación Social Femenil Tepepan, donde se encuentran mujeres sentenciadas y con problemas psiquiátricos. Los cuidados éticos observados en el estudio fueron: información de los objetivos a las entrevistadas, participación voluntaria, confidencialidad de la información, empleo de testigos, así como el derecho de abandonar el estudio y de no responder aquellas preguntas que les resultasen incómodas. El instrumento empleado tuvo un formato de entrevista semiestructurada con 242 preguntas que abarcan diversas áreas, entre ellas, el <<Cuestionario de Barreras hacia el tratamiento&gt;&gt; de Allen, que es autoadministrable y posee consistencia interna, validez de constructo y de contenido que fue adaptado por Romero (2002). En este trabajo se presentan únicamente los resultados de dicho cuestionario. Los resultados mostraron el siguiente perfil sociodemográfico en las entrevistadas: 45.5% se encontraba en el grupo de edad de 28 a 40 años; en cuanto a la escolaridad, las mujeres tenían una educación de 6 años o menos (41.3%), secundaria (36.2%), el estado civil fue en su mayoría solteras (48.6%) y en unión libre (21.6%); 50.7% tenía hijos menores de 18 años. Algunas otras características de esta muestra, como depresión, violencia, uso de alcohol y drogas se han reportado en otros trabajos. Del total de mujeres que alguna vez en la vida habían asistido a tratamiento, 52.6% (n = 112) mencionó algún tipo de barrera al tratamiento en adicciones. Un 29.1% (n = 62) de estas mujeres mencionó algún tipo de barrera al tratamiento por consumo de alcohol. El 44.1% (n=94) de ellas mencionó algún tipo de barrera al tratamiento por consumo de drogas. Por último, 39.2% (n = 44) mencionó algún tipo de barrera al tratamiento por ambos tipos de consumo. El análisis de la subescala a los tratamientos por variables sociodemográficas reveló mayores dificultades para ingresar a tratamiento entre las mujeres de 28 a 40 años de edad y entre quienes tenían hijos menores de 18 años. También se observaron diferencias estadísticamente significativas en relación con las variables tipo de delito (robo) y disponibilidad de los tratamientos. Los resultados de este estudio plantean al sector salud y a los servicios de salud mental retos para la atención oportuna en relación con el tratamiento y la rehabilitación de mujeres marginales. Asimismo, es crucial reconocer las inequidades de género cuando se diseñan estrategias de promoción a la salud. Sin dicha perspectiva, su efectividad se pone en riesgo y pueden llegar a aumentar las desigualdades de género. <![CDATA[<b>Predictors of short-term course in Mexican first-episode psychosis patients</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600005&lng=pt&nrm=iso&tlng=pt Background and objectives The identification of prognostic factors in patients with schizophrenia and related psychotic disorders should enhance our understanding of the aetiology of these disorders and improve their treatment. The first years following an initial episode of psychosis are a <<critical period&gt;&gt; for biological and psychosocial influences that affect future outcome. Both, short-term outcome and baseline predictors, have been defined by different measures, making the comparison among studies difficult. Studies of the predictive value of baseline demographic and clinical characteristics in the Mexican population are still limited. Hence, the present study aims to: 1. replicate the prognostic value of selected patient characteristics previously related to the short-term course of psychosis in Mexican first-episode psychosis patients, and 2. retrospectively assess their prognostic value in the prediction of diagnosis, presence of psychotic residual symptoms, and number of psychotic episodes at least three-years later. Methods Information on baseline predictor variables (sociodemographic, premorbid phase, context of the first episode, dimensions of psychopathology) and clinical outcome (diagnosis, residual symptomatology, psychotic episodes) was obtained from the clinical records of 51 patients with a short-term course of psychosis and whose available follow-up period was at least three years long (mean = 5.8,SD = 2.1). Results Poor premorbid adjustment and hospitalization at first psychotic episode were significant predictors of a schizophrenia diagnosis. Lower educational level and an insidious type of onset significantly predicted the presence of residual symptoms. Hospitalization at first psychotic episode and higher scores on the psychotic dimension at onset significantly predicted subsequent psychotic episodes. Discussion Low educational level increased the risk of residual symptoms, possibly because it hinders treatment continuity. Poor premorbid adjustment was related to a schizophrenia diagnosis at the follow-up assessment, supporting previous findings of their high ratings for premorbid impairment, including social withdrawal and dysfunctional peer relationship. Insidious onset was predictive of persistent residual symptoms; an association possibly mediated by the duration of untreated psychosis (DUP). Being hospitalized at first episode was a significant prognostic factor for schizophrenia diagnosis and multiple psychotic episodes; the severity and nature of symptoms at first episode that require hospitalization might account for these associations. Replicating previous findings, multiple-episode patients scored significantly higher than the single-episode patients on the psychoticism dimension. Most baseline factors did not predict diagnosis. This seems congruent with a dimensional view of psychosis suggesting that even though schizophrenic and non-schizophrenic psychoses are classified as separate families of disorders, they exist along a continuum of psychosis that crosses diagnostic boundaries, sharing aetiological and risk factors. Currently, both the amelioration of severe psychotic symptoms and the improvement of psychosocial functioning and quality of life are feasible aims. Symptom exacerbation and hospitalizations might cause cumulative deterioration and impair the patient's social reintegration. Thus, relapse prevention is an important objective in treatment. The identification of reliable predictors of illness course has significant implications for treatment and service planning. Conclusions The predictive value of several factors was replicated in this sample of patients with psychotic illnesses, although predictors seem to relate differently to the three short-term course measures. Comprehensively mapping the development and outcome of the first episode of psychosis requires the use of standardized measurement tools and the longitudinal assessment of multiple outcome measures.<hr/>Antecedentes y objetivos La identificación de factores pronósticos en pacientes con esquizofrenia y otros trastornos psicóticos relacionados podría facilitar la comprensión de la etiología de estos trastornos así como mejorar los tratamientos existentes. Los primeros años a partir del primer episodio psicótico son un <<período crítico&gt;&gt; en que factores biológicos y psicosociales influyen en el pronóstico futuro del trastorno. El hecho de que tanto el curso temprano como los predictores de línea base hayan sido definidos según diferentes medidas ha dificultado la comparación entre estudios. Los estudios sobre el valor predictivo de características clínicas y demográficas de línea base en población mexicana son aún escasos. En este sentido, el presente estudio tiene como objetivos: 1. replicar el valor pronóstico de algunas características del paciente previamente relacionadas con el curso temprano de la psicosis en una muestra de pacientes mexicanos con un primer episodio psicótico, y 2. evaluar retrospectivamente su valor como predictores del diagnóstico final, la presencia de síntomas psicóticos residuales y el número de episodios psicóticos ocurridos al menos tres años más tarde. Método Se recabó información acerca de variables predictoras de línea base (sociodemográficas, de fase premórbida, contexto del primer episodio, y dimensiones de la psicopatología) y sobre la evolución clínica (diagnóstico, síntomas psicóticos residuales, episodios psicóticos) de los expedientes de 51 pacientes con psicosis de curso temprano y con un tiempo de seguimiento disponible de al menos tres años (media = 5.8, SD = 2.1). Resultados Un ajuste premórbido pobre y haber sido hospitalizado en el primer episodio psicótico fueron predictores significativos de un diagnóstico de esquizofrenia. Un nivel educativo más bajo y un inicio insidioso de la enfermedad fueron predictores significativos de la presencia de síntomas residuales. La hospitalización durante el primer episodio psicótico y puntuaciones altas en la dimensión psicótica al inicio de la enfermedad fueron predictores significativos de episodios psicóticos posteriores. Discusión Se observó que un nivel educativo bajo incrementa el riesgo de síntomas residuales, posiblemente al dificultar la continuidad en el tratamiento. Se encontró que el ajuste premórbido pobre está relacionado con pacientes con esquizofrenia, corroborando así hallazgos previos sobre las altas puntuaciones de éstos en discapacidad premórbida, incluidos retraimiento social y relaciones disfuncionales con los pares. Un inicio insidioso predijo la presencia de síntomas residuales persistentes. La Duración de la Psicosis No Tratada (DPNT) puede actuar como mediador en tal asociación. La hospitalización en el primer episodio fue un factor pronóstico de diagnóstico de esquizofrenia y de múltiples episodios psicóticos. La gravedad y naturaleza de los síntomas en un primer episodio que requieran hospitalización es un factor a tomar en cuenta para explicar estas asociaciones. Los pacientes con episodios múltiples puntuaron más alto que los pacientes con un único episodio en la dimensión de psicoticismo. En concordancia con estudios previos, los pacientes con episodios psicóticos múltiples tuvieron puntuaciones más altas en la dimensión de psicoticismo que los pacientes con un episodio único de psicosis. La mayoría de los factores de línea base no predijeron el diagnóstico. Esto coincide con un enfoque dimensional de la psicosis, el cual sugiere que, aunque las psicosis esquizofrénicas y las no esquizofrénicas se clasifiquen como trastornos independientes, ambas existirían a lo largo de un continuo de psicosis, cruzando límites diagnósticos y compartiendo factores etiológicos y de riesgo en común. Actualmente, no sólo la mejoría de los síntomas psicóticos graves, sino también el buen funcionamiento psicosocial y la calidad de vida son metas viables. La exacerbación de síntomas y las hospitalizaciones pueden causar un deterioro acumulativo y afectar la reintegración social del paciente. Por ello, la prevención de recaídas es también un objetivo importante del tratamiento. La identificación de predictores confiables del curso de la enfermedad tiene importantes implicaciones para la planeación de tratamientos y servicios. Conclusiones Se replicó el valor predictivo de varios factores en esta muestra de pacientes con psicosis, aunque los predictores parecen relacionarse de manera diferente con cada una de las tres medidas de curso temprano. Por ello, se ha de poner atención en la medición y seguimiento estandarizados de diversas medidas del curso de la enfermedad a fin de trazar un mapa completo de la evolución y el pronóstico de un primer episodio de psicosis. <![CDATA[<b>The levels of psychological functioning of personality and the mechanisms of defense</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600006&lng=pt&nrm=iso&tlng=pt Otto Kernberg states three types of personality organizations, also named psychological functional levels. They reflect the patient's predominant psychological characteristics: identity integration grade, defense mechanisms, and reality test. In mental disorders, the predominant defensive influences significantly in the severity and evolution of the suffering. Objectives The objective of the actual study was to determine the usage of defense mechanisms by patients with some mental disorder, grouping them according to personality organization levels or psychological functioning and the DSM-IV-TR Axis II diagnostic. Sample The sample included two groups: a) 1 02 hospitalized patients in the Instituto Nacional de Psiquiatría, 20 males and 82 females. b) A control group formed by 125 individuals, 48 males and 77 females; in all cases, they lived in Distrito Federal or Estado de México. Method The sample of this study was evaluated with the Defensive Questionnaire (DSQ-40) and the Personality Diagnostic Questionnaire (PDQ-4 + ); both instruments were applied as soon as patients were admitted to the hospital. The concepts of borderline psychological functioning and borderline personality disorder make reference to: The levels of personality organization or borderline psychological functioning characterized by an identity integration failure named identity diffusion, habitually reality judgment conserving and low level defenses supported on the splitting. b) The patients that were diagnosed with borderline personality disorder in agreement with the DSM-IV-TR. According to the personality organization, the psychotic disorders were grouped in the psychotic functioning level; the rest of the patients that suffered some anxiety or mood disorders were included in the borderline functioning level when they had also a diagnosis of borderline, narcissistic, antisocial, paranoid, schizoid, schizotypal, avoidant, dependent or histrionic personality disorder; in the neurotic functioning level those patients without personality disorder. The members of the control group were included in different academic level, labor and social scopes during the same period. Results The patients with a low level of personality organization (psychotic or borderline personality organization) used predominantly the immature or primitive defense mechanisms; patients with a high level of personality organization (neurotic level of psychological functioning) and members of the control group used predominantly mature or advanced defense mechanisms. Derived from the factorial analysis, three levels of defensive were determined: mature/advanced, neurotic and immature/primitive. In the mature/advanced defensive, the members of the control group were those that scored higher, followed by the psychotic patients and borderline. The scores of the neurotic defensive were higher in the borderline and psychotic groups than the control group. In the immature/primitive defensive, the borderline patients had higher scores than the psychotic and control group. The patients that were diagnosed through the PDQ-4+ with borderline personality disorder in agreement with the DSM-IV-TR had lower scores in the mature/advance defensive and higher than the control group in neurotic and immature/primitive defensive . The characteristics of personality of clusters A and B correlated positively with the following defensive s: immature/ primitive and neurotic and negatively with the mature/advanced defensive . The relation between the defensive s and the characteristics of personality of cluster C was negative in the defensive mature/advanced and positive in the neurotic and immature/ primitive. Conclusions: Through these findings a hierarchy between the levels of psychological functioning can be established, so that the lower the level of psychological functioning (borderline or psychotic), the higher is the use of immature mechanisms of defense and vice versa. The level of high psychological functioning (neurotic) used mature mechanisms of defense mainly; the borderline and psychotic levels of psychological functioning had major use of immature defenses, such as projection and autistic fantasy.<hr/>Los mecanismos de defensa son los elementos fundamentales de la organización de la personalidad, junto con la constancia objetal y el juicio de realidad. En los trastornos mentales, el estilo defensivo predominante influye significativamente en la gravedad y evolución del padecimiento. Objetivos El objetivo de este estudio fue determinar la relación existente entre los mecanismos de defensa, los trastornos de la personalidad y los niveles de funcionamiento psicológico (organización de la personalidad tipo neurótica, límite o psicótica) propuestos por Kernberg. Muestra La muestra del estudio estuvo constituida por dos grupos: a) Un grupo de 102 pacientes psiquiátricos hospitalizados, 20 del sexo masculino y 82 del femenino, provenientes del Instituto Nacional de Psiquiatría Ramón de la Fuente. b) Un grupo control, constituido por 1 25 sujetos, 48 hombres y 77 mujeres, en su mayoría residentes del Distrito Federal o del Estado de México. Método La población de este estudio fue evaluada con el Cuestionario de Estilos Defensivos (DSQ-40) y el Cuestionario Diagnóstico de la Personalidad (PDQ-4 + ) para determinar el uso de los mecanismos de defensa y detectar los trastornos de la personalidad, respectivamente. A los pacientes se les aplicaron ambos instrumentos al momento de su ingreso y se les agrupó en alguno de los tres niveles de funcionamiento psicológico de Kernberg. Los conceptos nivel de funcionamiento psicológico límite y trastorno límite de la personalidad hacen referencia a: a) La organización de la personalidad o nivel de funcionamiento límite caracterizada por la difusión de identidad, habitualmente conservación de la prueba de realidad y mecanismos de defensa basados en la escisión. b) El trastorno límite de la personalidad descrito por la Asociación Psiquiátrica Americana en el DSM-IV-TR. De acuerdo con la organización de la personalidad, los pacientes esquizofrénicos y con otras psicosis quedaron en el nivel de funcionamiento psicótico. Los pacientes que sufrían algún trastorno de ansiedad o del estado de ánimo se incluyeron en el nivel de funcionamiento límite o borderline cuando también tenían diagnóstico de trastornos de personalidad límite, narcisista, antisocial, paranoide, esquizoide, esquizotípico, evitativo, dependiente e histriónico; en el nivel de funcionamiento neurótico se incluyeron los pacientes con los trastornos mencionados, que no tenían trastorno de personalidad o bien cuyo diagnóstico fue de trastorno obsesivo-compulsivo de la personalidad. Los sujetos que sirvieron como controles fueron captados en distintos ámbitos escolares, laborales y sociales durante el mismo periodo. Resultados Los pacientes pertenecientes a los niveles de funcionamiento psicológico menores (psicótico o límite) usaron más los mecanismos de defensa inmaduros en comparación con los pertenecientes al nivel de funcionamiento psicológico de mayor nivel (neurótico) y que los sujetos controles. Se determinaron tres estilos defensivos: maduro/ avanzado, neurótico e inmaduro/primitivo. En el estilo maduro/ avanzado los sujetos del grupo control fueron los que puntuaron más alto, seguidos de los pacientes con nivel de funcionamiento psicológico psicótico y límite. Las puntuaciones del estilo defensivo neurótico fueron mayores en los grupos límite y psicótico que en el grupo control. En el estilo defensivo inmaduro/primitivo, los pacientes límites tuvieron puntuaciones mayores que los grupos psicótico y control. El grupo control puntuó más alto que el límite en sublimación, humor, anticipación y supresión, y que el psicótico en humor y supresión. El grupo de funcionamiento límite tuvo puntuaciones mayores que el grupo control en anulación, aislamiento, racionalización, proyección, agresión pasiva, exoactuación, fantasía autista, escisión y somatización. En cambio, puntuaron más alto que el grupo psicótico en supresión, agresión pasiva y somatización. El grupo psicótico tuvo puntuaciones mayores que el grupo límite en sublimación, anticipación y formación reactiva, y que el grupo control en anulación, desplazamiento, proyección y fantasía autista. Los pacientes diagnosticados a través del PDQ-4+ con trastorno límite de personalidad de acuerdo con el DSM-IV-TR tuvieron puntuaciones menores en el estilo defensivo maduro/avanzado que el grupo control pero mayores en los estilos defensivos neurótico e inmaduro/ primitivo. En el análisis individual de cada mecanismo de defensa se encontró que el grupo control tuvo mayores puntuaciones en sublimación, humor, anticipación, supresión y disociación que el grupo de pacientes con trastorno límite de la personalidad. Éstos puntuaron más alto en desplazamiento, racionalización, aislamiento, proyección, escisión, exoactuación, agresión pasiva, devaluación, fantasía autista, negación y somatización. Cuando se determinó el uso de las defensas de acuerdo con el diagnóstico de trastornos de la personalidad pertenecientes a los clusters A y B, se observó un mayor uso de los mecanismos de defensa basados en la escisión; de éstos, la fantasía autista fue la que tuvo mayor valor predictivo. Por el contrario, los trastornos de la personalidad del cluster C estuvieron asociados a los mecanismos de defensa de la esfera de la represión. Conclusiones Los resultados dan sustento empírico a la organización de la personalidad propuesta por Kernberg sobre los tres niveles de funcionamiento psicológico y a la vez demuestran la relación entre los trastornos de la personalidad y los mecanismos de defensa. El mecanismo de defensa denominado fantasía autista resultó ser un factor explicativo y predictivo de las características de la personalidad de los clusters A y B y del trastorno límite de la personalidad, en específico. <![CDATA[<b>Comparative analysis of attributional and self-esteem in a sample of patients with delusions and control subjets</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600007&lng=pt&nrm=iso&tlng=pt Introduction The attributional along with the self-esteem (that plays a central role in the development and maintenance of the pathological state) is a very important mediating element in the delusion, so we find the necessity to realise basic studies of these processes. In the field of psychology, and mainly in the personality area, the atributional has a great relevance, when understanding the causal attributions like mechanisms of facing that guide the conduct of the subject. In this way, we see the importance that supposes the study of the dysfunctional attribution to be able to replace it on the other adaptive, mainly in the pathologies where delusions beliefs exist. In the present investigation the influence has been analyzed that carries out the variable attributional and the self-esteem in the delusional ideas (defined by the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders [DSM-IV] as <<false belief based on the realization of incorrect inferences about external reality, beliefs that are held firmly believe despite of almost everyone else, and despite of constitutes an obvious proof or evidence otherwise indisputable&gt;&gt;) in a sample of delusional patients in comparison with a group control. Most of the research, focus on the dimension of <<Internal&gt;&gt; in this study (following previous research), is to examine attributional biases in the reasoning of delirious patients. Therefore, the departure hypotheses are the following: a) the delusional patients, more than the normal subjects, will realise in their social reasoning more external attributions for the negative events that stop the positives; b) the delusional patients, like the control group, tend to realise global and excessively stable attributions, as much for positive events as for negative events; and c) the delusional patients in comparison with the control group will indicate a high self-esteem. Patients and methods To carry out this research both self-esteem and attributional have been tested in a sample of 20 delusional in-patients (85% are men and 15% women of average age of 36.20 years) entered the unit of Rehabilitation of a Psychiatric Hospital of Santiago de Compostela (Spain) and have been compared to 40 normal control subject in age and sex with the experimental group that do not own psychiatric history, no upheaval that requires treatment. The criteria of inclusion have been the following: a) all of the patients were entered the unit of Rehabilitation, b) the patients had delusional ideas at the moment of the tests, c) their diagnosis fulfilled the criteria according to DSM-IV for paranoid schizophrenia (16 patients) and delusions upheaval (paranoid) (4 patients), d) the ages of the patients had to be included between 20 and 50 years, e) none of the patients had a history of drug use, f) patient did not show evidence of organic brain disorders, g) all of them had a score in items 1 (delusion), 5 (magnitude), and 6 (mistrust/damage) in the positive scale of PANSS (PANSS-P) of more than 3, and h) all the patients had more than 5 years of disease. One is comparative, observational, and cross-sectional and homodemic a study according to the propose classification by Feinstein and with a design of cases and controls. The instruments applied in the study were: a) Rosenberg Self-esteem Scale (EA), is an instrument for assessing the patient's global self-esteem; b) Attributional Questionnaire (ASQ), which is a self-administered questionnaire consisting of twelve situations, six positive (success) and six negative (failure), against which the subject must indicate the causes they attribute its occurrence; and c) Positive and Negative Syndrome Scale for Schizophrenia (PANSS), suitable for evaluation of positive and negative symptoms in schizophrenia. Of the thirty items included in the PANSS, seven are positive scale (PANSS-P), seven the negative scale (PANSS-N), and the sixteen remaining general psychopathology scale (PANSS-PG). All the instruments used for the study, count on their corresponding data of reliability and validity. In this investigation a descriptive analysis of the object of study has been carried out variable, which provided us the frequency allocation, percentage, averages, medians and standard deviations for each of them. Results The results of this investigation show that the delusional patients realised more external attributions for the negative events that the group normal control, and more internal for the positives. The delusional patients realised a causal attribution in stability and globality for the negative events similar to the one of the normal ones. Nevertheless, before positive events have been significant differences between both groups in relation to the stability, not thus for the globality. Also the delusional patients, like the group normal control, indicated a high self-esteem. In the statistic analysis has not been significant differences in self-esteem between the delusional group and the group control that the hypothesis supports that the delusional ones have a high self-esteem with respect to the normal ones. Conclusion The hypothesis raised by Bentall has not been able to state in this investigation, since when analyzing the variable self-esteem we observed that their scores are similar to the group control of normal. According to the atribucional , one concludes that the delusional subjects tend to blame their failures and errors to the other people or other circumstances. On the other hand, when they are successful in some situation, they consider that it must to them themselves, attributing the favourable events to internal level. The conclusions of the analysis of the globality dimension, which determines the temporary generalization of the expectation, do not fulfil the hypothesis in which it affirmed that the delusional subjects, like the normal ones, excessively realised global attributions as much for positive facts as for negative, but do not indicate an exaggerated slant towards the excessive globality. The hypothesis raised by Bentall that the delusion reflect a defensive atribucional , which protects the individual against feelings of low self-esteem, has not been possible to state in this investigation, since when analyzing the variable self-esteem we observed that significant differences in the delusional patients do not exist, since their scores are similar to the group control, showing a both high self-esteem. By all this, it is possible to be concluded that it enters the delusional patients and the group control only exists significant differences taking care of the atribucional of each group. However, such studies contribute along with other made in the understanding of these disorders and consequently to the development of effective psychological program with the aim of improving the symptoms of these patients and even in other pathologies.<hr/>Introducción El estilo atribucional y la autoestima (que cumple un papel central en el desarrollo y mantenimiento del estado patológico) son elementos mediadores muy importantes en el delirio. De ahí la necesidad de realizar estudios básicos de dichos procesos. En el campo de la psicología, y en concreto en el área de personalidad, el estilo atribucional es de gran relevancia al entender las atribuciones causales como mecanismos de afrontamiento que guían la conducta del sujeto. Por ello, la importancia que supone el estudio de la atribución disfuncional para poder sustituirla por otra adaptativa, sobre todo en las patologías donde existen creencias delirantes. En la presente investigación se ha analizado el papel que desempeñan la variable estilo atribucional y la autoestima en las ideas del irantes en una muestra de pacientes delirantes en comparación con un grupo control. Pacientes y métodos En esta investigación se ha examinado la autoestima y los sesgos atribucionales en una muestra de 20 pacientes delirantes (85% son hombres y 15% mujeres de edad media de 36.20 años) ingresados en la unidad de Rehabilitación de un Hospital Psiquiátrico de Santiago de Compostela (España) y se ha comparado con 40 sujetos control normales igualados en edad y sexo con el grupo experimental que no poseen historia psiquiátrica, ni ningún trastorno que requiera tratamiento. Se trata de un estudio comparativo, observacional, transversal y homodémico según la clasificación propuesta por Feinstein y con un diseño de casos y controles. Los instrumentos aplicados en el estudio fueron: a) la Escala de Autoestima de Rosenberg (Rosenberg Self-esteem Scale, EA), b) el Cuestionario de Estilo Atribucional (Attributional Questionnaire, ASQ) y c) la Escala de Síndrome Positivo y Negativo en la Esquizofrenia (Positive and Negative Syndrome Scale for Schizophrenia, PANSS). Todos los instrumentos empleados para el estudio cuentan con sus correspondientes datos de fiabilidad y validez. Resultados Los resultados de esta investigación muestran que los pacientes delirantes realizaron atribuciones más externas para los eventos negativos que el grupo control normal, y más internas para los positivos. Los pacientes delirantes realizaron una atribución causal en estabilidad y globalidad para los sucesos negativos similar a la de los normales. Sin embargo, ante eventos positivos se han encontrado diferencias significativas entre ambos grupos en relación con la estabilidad, no así para la globalidad. Asimismo, los pacientes delirantes, al igual que el grupo control normal, manifestaron una alta autoestima. Conclusión La hipótesis planteada por Bentall no se ha podido constatar en esta investigación, ya que al analizar la variable autoestima observamos que sus puntuaciones son similares al grupo control de sujetos normales. Según el estilo atribucional, se concluye que los sujetos delirantes tienden a culpar por sus fallos y errores a las demás personas o a otras circunstancias. Por el contrario, cuando ellos tienen éxito en alguna situación, consideran que se debe a ellos mismos, y atribuyen los eventos favorables a nivel interno. Las conclusiones del análisis de la dimensión globalidad, la cual determina la generalización temporal de la expectativa, no cumplen la hipótesis en la cual se afirmaba que los sujetos delirantes, al igual que los normales, realizaban atribuciones excesivamente globales tanto para hechos positivos como para negativos, pero no manifiestan un sesgo exagerado hacia la excesiva globalidad. <![CDATA[<b>Brain, drugs and genes</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600008&lng=pt&nrm=iso&tlng=pt In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle A9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It actually contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, A9-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effects that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of an interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal functions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated.<hr/>En este segundo artículo sobre el tema reseñamos brevemente las drogas de abuso ilícitas. Describiremos también cómo la genética contribuye en forma importante en el desarrollo de la adicción. La marihuana (Cannabis sativa) es una de las drogas más populares entre los jóvenes. Se presenta para su consumo en dos formas: hachís, como un triturado de la planta seca y como aceite. Una vez consumida, sus efectos tardan en aparecer según la vía de administración. Por ejemplo, cuando se inhala, sus efectos aparecen en unos cuantos segundos. Después de que el principio activo de la marihuana (A9-THC) llega al cerebro y se une a sus receptores (CB1), produce euforia seguida de relajación, se perciben más intensamente los olores, los sabores y los sonidos y parece que el tiempo pasa lentamente. Su consumo, al igual que todas las drogas de abuso, tiene efectos adversos. Sin embargo, la marihuana cuenta con un potencial uso en la medicina por sus propiedades antieméticas, orexigénicas y analgésicas. La heroína es derivada de la morfina (ingrediente activo del opio, Papaver somniferum). El opio se fuma o se utiliza como un extracto disuelto en alcohol (láudano), y la heroína se aspira o fuma. Sus efectos aparecen rápidamente e incluyen euforia, aumento de la energía, supresión del hambre, analgesia y somnolencia. La heroína, así como el opio y la morfina, ejercen su efecto a través de los receptores opioides. Su consumo deteriora el hígado, los riñones, los pulmones y el corazón. La cocaína (Erythroxylum coca) es una droga estimulante altamente adictiva. Al consumirla se experimenta mejoría de la autoestima y la auto-confianza, acompañada de excitación. Estos efectos son inmediatos y duran entre 30 y 60 minutos y son consecuencia de la inhibición de la recaptura de dopamina. Adicionalmente la cocaína inhibe el apetito y el sueño. Sus efectos adversos son la contracción de los vasos sanguíneos, espasmos musculares, dolor de pecho, embolias o derrames cerebrales, aumento en la frecuencia cardiaca y muerte. La metanfetamina se sintetiza fácilmente a partir de la anfetamina (derivado de la efedrina), lo que facilita su fabricación en laboratorios clandestinos. Cuando se fuma o se inyecta por vía intravenosa produce una sensación sumamente placentera (<<rush&gt;&gt; o <<flash&gt;&gt;), que dura pocos minutos. Consumida por vía oral o inhalada produce una euforia de mayor duración. Estos efectos son consecuencia del incremento de la liberación de dopamina. Entre los efectos adversos aparecen insomnio, incremento en la actividad física (por lo cual suele ser consumida por deportistas) y disminución del apetito (este es un motivo adicional de consumo), incremento de la temperatura corporal, aumento en el ritmo cardíaco y la presión arterial. La 3,4-metilenedioximetanfetamina, MDMA o éxtasis, es estimulante y psicodélico. Produce un efecto vigorizante, distorsiona la percepción, incluida la del tiempo. Su principal efecto es inhibir el trasportador de serotonina, pero también aumenta la disponibilidad de noradrenalina y dopamina. La adicción depende de factores sociales y psicológicos, pero la contribución genética es muy importante. Nuestros genes pueden hacernos vulnerables al consumo de drogas. Algunos polimorfismos de diversos genes nos pueden volver sensibles a la adicción o incluso dificultar la eficiencia de los tratamientos orientados a la rehabilitación. Uno de los polimorfismos más estudiados es el de las enzimas hepáticas (CYP450), asociados a la vulnerabilidad para la adicción al tabaco, el alcohol y la heroína. Adicionalmente, debemos considerar que nuestro material genético responde a los estímulos ambientales (epigénesis), de tal forma que condiciones ambientales inadecuadas, v. gr. pobre cuidado maternal, puede cambiar nuestra conducta (baja respuesta al estrés) y tornarnos vulnerables a la adicción. <![CDATA[<b>Music, languaje and emotion</b>: <b>a brain approach</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600009&lng=pt&nrm=iso&tlng=pt In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle A9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It actually contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, A9-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effects that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of an interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal functions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated.<hr/>En este segundo artículo sobre el tema reseñamos brevemente las drogas de abuso ilícitas. Describiremos también cómo la genética contribuye en forma importante en el desarrollo de la adicción. La marihuana (Cannabis sativa) es una de las drogas más populares entre los jóvenes. Se presenta para su consumo en dos formas: hachís, como un triturado de la planta seca y como aceite. Una vez consumida, sus efectos tardan en aparecer según la vía de administración. Por ejemplo, cuando se inhala, sus efectos aparecen en unos cuantos segundos. Después de que el principio activo de la marihuana (A9-THC) llega al cerebro y se une a sus receptores (CB1), produce euforia seguida de relajación, se perciben más intensamente los olores, los sabores y los sonidos y parece que el tiempo pasa lentamente. Su consumo, al igual que todas las drogas de abuso, tiene efectos adversos. Sin embargo, la marihuana cuenta con un potencial uso en la medicina por sus propiedades antieméticas, orexigénicas y analgésicas. La heroína es derivada de la morfina (ingrediente activo del opio, Papaver somniferum). El opio se fuma o se utiliza como un extracto disuelto en alcohol (láudano), y la heroína se aspira o fuma. Sus efectos aparecen rápidamente e incluyen euforia, aumento de la energía, supresión del hambre, analgesia y somnolencia. La heroína, así como el opio y la morfina, ejercen su efecto a través de los receptores opioides. Su consumo deteriora el hígado, los riñones, los pulmones y el corazón. La cocaína (Erythroxylum coca) es una droga estimulante altamente adictiva. Al consumirla se experimenta mejoría de la autoestima y la auto-confianza, acompañada de excitación. Estos efectos son inmediatos y duran entre 30 y 60 minutos y son consecuencia de la inhibición de la recaptura de dopamina. Adicionalmente la cocaína inhibe el apetito y el sueño. Sus efectos adversos son la contracción de los vasos sanguíneos, espasmos musculares, dolor de pecho, embolias o derrames cerebrales, aumento en la frecuencia cardiaca y muerte. La metanfetamina se sintetiza fácilmente a partir de la anfetamina (derivado de la efedrina), lo que facilita su fabricación en laboratorios clandestinos. Cuando se fuma o se inyecta por vía intravenosa produce una sensación sumamente placentera (<<rush&gt;&gt; o <<flash&gt;&gt;), que dura pocos minutos. Consumida por vía oral o inhalada produce una euforia de mayor duración. Estos efectos son consecuencia del incremento de la liberación de dopamina. Entre los efectos adversos aparecen insomnio, incremento en la actividad física (por lo cual suele ser consumida por deportistas) y disminución del apetito (este es un motivo adicional de consumo), incremento de la temperatura corporal, aumento en el ritmo cardíaco y la presión arterial. La 3,4-metilenedioximetanfetamina, MDMA o éxtasis, es estimulante y psicodélico. Produce un efecto vigorizante, distorsiona la percepción, incluida la del tiempo. Su principal efecto es inhibir el trasportador de serotonina, pero también aumenta la disponibilidad de noradrenalina y dopamina. La adicción depende de factores sociales y psicológicos, pero la contribución genética es muy importante. Nuestros genes pueden hacernos vulnerables al consumo de drogas. Algunos polimorfismos de diversos genes nos pueden volver sensibles a la adicción o incluso dificultar la eficiencia de los tratamientos orientados a la rehabilitación. Uno de los polimorfismos más estudiados es el de las enzimas hepáticas (CYP450), asociados a la vulnerabilidad para la adicción al tabaco, el alcohol y la heroína. Adicionalmente, debemos considerar que nuestro material genético responde a los estímulos ambientales (epigénesis), de tal forma que condiciones ambientales inadecuadas, v. gr. pobre cuidado maternal, puede cambiar nuestra conducta (baja respuesta al estrés) y tornarnos vulnerables a la adicción. <![CDATA[<b>Pronunciamiento de la Academia Nacional de Medicina de México ante el consumo de sustancias psicoactivas y los trastornos derivados de su abuso</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600010&lng=pt&nrm=iso&tlng=pt In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle A9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It actually contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, A9-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effects that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of an interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal functions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated.<hr/>En este segundo artículo sobre el tema reseñamos brevemente las drogas de abuso ilícitas. Describiremos también cómo la genética contribuye en forma importante en el desarrollo de la adicción. La marihuana (Cannabis sativa) es una de las drogas más populares entre los jóvenes. Se presenta para su consumo en dos formas: hachís, como un triturado de la planta seca y como aceite. Una vez consumida, sus efectos tardan en aparecer según la vía de administración. Por ejemplo, cuando se inhala, sus efectos aparecen en unos cuantos segundos. Después de que el principio activo de la marihuana (A9-THC) llega al cerebro y se une a sus receptores (CB1), produce euforia seguida de relajación, se perciben más intensamente los olores, los sabores y los sonidos y parece que el tiempo pasa lentamente. Su consumo, al igual que todas las drogas de abuso, tiene efectos adversos. Sin embargo, la marihuana cuenta con un potencial uso en la medicina por sus propiedades antieméticas, orexigénicas y analgésicas. La heroína es derivada de la morfina (ingrediente activo del opio, Papaver somniferum). El opio se fuma o se utiliza como un extracto disuelto en alcohol (láudano), y la heroína se aspira o fuma. Sus efectos aparecen rápidamente e incluyen euforia, aumento de la energía, supresión del hambre, analgesia y somnolencia. La heroína, así como el opio y la morfina, ejercen su efecto a través de los receptores opioides. Su consumo deteriora el hígado, los riñones, los pulmones y el corazón. La cocaína (Erythroxylum coca) es una droga estimulante altamente adictiva. Al consumirla se experimenta mejoría de la autoestima y la auto-confianza, acompañada de excitación. Estos efectos son inmediatos y duran entre 30 y 60 minutos y son consecuencia de la inhibición de la recaptura de dopamina. Adicionalmente la cocaína inhibe el apetito y el sueño. Sus efectos adversos son la contracción de los vasos sanguíneos, espasmos musculares, dolor de pecho, embolias o derrames cerebrales, aumento en la frecuencia cardiaca y muerte. La metanfetamina se sintetiza fácilmente a partir de la anfetamina (derivado de la efedrina), lo que facilita su fabricación en laboratorios clandestinos. Cuando se fuma o se inyecta por vía intravenosa produce una sensación sumamente placentera (<<rush&gt;&gt; o <<flash&gt;&gt;), que dura pocos minutos. Consumida por vía oral o inhalada produce una euforia de mayor duración. Estos efectos son consecuencia del incremento de la liberación de dopamina. Entre los efectos adversos aparecen insomnio, incremento en la actividad física (por lo cual suele ser consumida por deportistas) y disminución del apetito (este es un motivo adicional de consumo), incremento de la temperatura corporal, aumento en el ritmo cardíaco y la presión arterial. La 3,4-metilenedioximetanfetamina, MDMA o éxtasis, es estimulante y psicodélico. Produce un efecto vigorizante, distorsiona la percepción, incluida la del tiempo. Su principal efecto es inhibir el trasportador de serotonina, pero también aumenta la disponibilidad de noradrenalina y dopamina. La adicción depende de factores sociales y psicológicos, pero la contribución genética es muy importante. Nuestros genes pueden hacernos vulnerables al consumo de drogas. Algunos polimorfismos de diversos genes nos pueden volver sensibles a la adicción o incluso dificultar la eficiencia de los tratamientos orientados a la rehabilitación. Uno de los polimorfismos más estudiados es el de las enzimas hepáticas (CYP450), asociados a la vulnerabilidad para la adicción al tabaco, el alcohol y la heroína. Adicionalmente, debemos considerar que nuestro material genético responde a los estímulos ambientales (epigénesis), de tal forma que condiciones ambientales inadecuadas, v. gr. pobre cuidado maternal, puede cambiar nuestra conducta (baja respuesta al estrés) y tornarnos vulnerables a la adicción. <![CDATA[<b>In memoriam Dr. Carlos José Rodríguez Ajenjo (1949-2010)</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600011&lng=pt&nrm=iso&tlng=pt In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle A9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It actually contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, A9-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effects that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of an interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal functions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated.<hr/>En este segundo artículo sobre el tema reseñamos brevemente las drogas de abuso ilícitas. Describiremos también cómo la genética contribuye en forma importante en el desarrollo de la adicción. La marihuana (Cannabis sativa) es una de las drogas más populares entre los jóvenes. Se presenta para su consumo en dos formas: hachís, como un triturado de la planta seca y como aceite. Una vez consumida, sus efectos tardan en aparecer según la vía de administración. Por ejemplo, cuando se inhala, sus efectos aparecen en unos cuantos segundos. Después de que el principio activo de la marihuana (A9-THC) llega al cerebro y se une a sus receptores (CB1), produce euforia seguida de relajación, se perciben más intensamente los olores, los sabores y los sonidos y parece que el tiempo pasa lentamente. Su consumo, al igual que todas las drogas de abuso, tiene efectos adversos. Sin embargo, la marihuana cuenta con un potencial uso en la medicina por sus propiedades antieméticas, orexigénicas y analgésicas. La heroína es derivada de la morfina (ingrediente activo del opio, Papaver somniferum). El opio se fuma o se utiliza como un extracto disuelto en alcohol (láudano), y la heroína se aspira o fuma. Sus efectos aparecen rápidamente e incluyen euforia, aumento de la energía, supresión del hambre, analgesia y somnolencia. La heroína, así como el opio y la morfina, ejercen su efecto a través de los receptores opioides. Su consumo deteriora el hígado, los riñones, los pulmones y el corazón. La cocaína (Erythroxylum coca) es una droga estimulante altamente adictiva. Al consumirla se experimenta mejoría de la autoestima y la auto-confianza, acompañada de excitación. Estos efectos son inmediatos y duran entre 30 y 60 minutos y son consecuencia de la inhibición de la recaptura de dopamina. Adicionalmente la cocaína inhibe el apetito y el sueño. Sus efectos adversos son la contracción de los vasos sanguíneos, espasmos musculares, dolor de pecho, embolias o derrames cerebrales, aumento en la frecuencia cardiaca y muerte. La metanfetamina se sintetiza fácilmente a partir de la anfetamina (derivado de la efedrina), lo que facilita su fabricación en laboratorios clandestinos. Cuando se fuma o se inyecta por vía intravenosa produce una sensación sumamente placentera (<<rush&gt;&gt; o <<flash&gt;&gt;), que dura pocos minutos. Consumida por vía oral o inhalada produce una euforia de mayor duración. Estos efectos son consecuencia del incremento de la liberación de dopamina. Entre los efectos adversos aparecen insomnio, incremento en la actividad física (por lo cual suele ser consumida por deportistas) y disminución del apetito (este es un motivo adicional de consumo), incremento de la temperatura corporal, aumento en el ritmo cardíaco y la presión arterial. La 3,4-metilenedioximetanfetamina, MDMA o éxtasis, es estimulante y psicodélico. Produce un efecto vigorizante, distorsiona la percepción, incluida la del tiempo. Su principal efecto es inhibir el trasportador de serotonina, pero también aumenta la disponibilidad de noradrenalina y dopamina. La adicción depende de factores sociales y psicológicos, pero la contribución genética es muy importante. Nuestros genes pueden hacernos vulnerables al consumo de drogas. Algunos polimorfismos de diversos genes nos pueden volver sensibles a la adicción o incluso dificultar la eficiencia de los tratamientos orientados a la rehabilitación. Uno de los polimorfismos más estudiados es el de las enzimas hepáticas (CYP450), asociados a la vulnerabilidad para la adicción al tabaco, el alcohol y la heroína. Adicionalmente, debemos considerar que nuestro material genético responde a los estímulos ambientales (epigénesis), de tal forma que condiciones ambientales inadecuadas, v. gr. pobre cuidado maternal, puede cambiar nuestra conducta (baja respuesta al estrés) y tornarnos vulnerables a la adicción. <![CDATA[<b>In memoriam Prof. René Tissot (1927-2010)</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600012&lng=pt&nrm=iso&tlng=pt In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle A9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It actually contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, A9-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effects that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of an interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal functions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated.<hr/>En este segundo artículo sobre el tema reseñamos brevemente las drogas de abuso ilícitas. Describiremos también cómo la genética contribuye en forma importante en el desarrollo de la adicción. La marihuana (Cannabis sativa) es una de las drogas más populares entre los jóvenes. Se presenta para su consumo en dos formas: hachís, como un triturado de la planta seca y como aceite. Una vez consumida, sus efectos tardan en aparecer según la vía de administración. Por ejemplo, cuando se inhala, sus efectos aparecen en unos cuantos segundos. Después de que el principio activo de la marihuana (A9-THC) llega al cerebro y se une a sus receptores (CB1), produce euforia seguida de relajación, se perciben más intensamente los olores, los sabores y los sonidos y parece que el tiempo pasa lentamente. Su consumo, al igual que todas las drogas de abuso, tiene efectos adversos. Sin embargo, la marihuana cuenta con un potencial uso en la medicina por sus propiedades antieméticas, orexigénicas y analgésicas. La heroína es derivada de la morfina (ingrediente activo del opio, Papaver somniferum). El opio se fuma o se utiliza como un extracto disuelto en alcohol (láudano), y la heroína se aspira o fuma. Sus efectos aparecen rápidamente e incluyen euforia, aumento de la energía, supresión del hambre, analgesia y somnolencia. La heroína, así como el opio y la morfina, ejercen su efecto a través de los receptores opioides. Su consumo deteriora el hígado, los riñones, los pulmones y el corazón. La cocaína (Erythroxylum coca) es una droga estimulante altamente adictiva. Al consumirla se experimenta mejoría de la autoestima y la auto-confianza, acompañada de excitación. Estos efectos son inmediatos y duran entre 30 y 60 minutos y son consecuencia de la inhibición de la recaptura de dopamina. Adicionalmente la cocaína inhibe el apetito y el sueño. Sus efectos adversos son la contracción de los vasos sanguíneos, espasmos musculares, dolor de pecho, embolias o derrames cerebrales, aumento en la frecuencia cardiaca y muerte. La metanfetamina se sintetiza fácilmente a partir de la anfetamina (derivado de la efedrina), lo que facilita su fabricación en laboratorios clandestinos. Cuando se fuma o se inyecta por vía intravenosa produce una sensación sumamente placentera (<<rush&gt;&gt; o <<flash&gt;&gt;), que dura pocos minutos. Consumida por vía oral o inhalada produce una euforia de mayor duración. Estos efectos son consecuencia del incremento de la liberación de dopamina. Entre los efectos adversos aparecen insomnio, incremento en la actividad física (por lo cual suele ser consumida por deportistas) y disminución del apetito (este es un motivo adicional de consumo), incremento de la temperatura corporal, aumento en el ritmo cardíaco y la presión arterial. La 3,4-metilenedioximetanfetamina, MDMA o éxtasis, es estimulante y psicodélico. Produce un efecto vigorizante, distorsiona la percepción, incluida la del tiempo. Su principal efecto es inhibir el trasportador de serotonina, pero también aumenta la disponibilidad de noradrenalina y dopamina. La adicción depende de factores sociales y psicológicos, pero la contribución genética es muy importante. Nuestros genes pueden hacernos vulnerables al consumo de drogas. Algunos polimorfismos de diversos genes nos pueden volver sensibles a la adicción o incluso dificultar la eficiencia de los tratamientos orientados a la rehabilitación. Uno de los polimorfismos más estudiados es el de las enzimas hepáticas (CYP450), asociados a la vulnerabilidad para la adicción al tabaco, el alcohol y la heroína. Adicionalmente, debemos considerar que nuestro material genético responde a los estímulos ambientales (epigénesis), de tal forma que condiciones ambientales inadecuadas, v. gr. pobre cuidado maternal, puede cambiar nuestra conducta (baja respuesta al estrés) y tornarnos vulnerables a la adicción. <![CDATA[<b>Autoevaluación</b>]]> http://www.scielo.org.mx/scielo.php?script=sci_arttext&pid=S0185-33252010000600013&lng=pt&nrm=iso&tlng=pt In this second paper of the Brain, Drugs and Genes review we would like to discuss illicit drugs and the genetics that may predispose subjects to addiction. We describe the effects, action sites and pathophysiological consequences of the use of these illicit drugs. The drugs that are reviewed are marijuana, heroin, cocaine, methamphetamine and 3,4-methylenedioxymethamphetamine or MDMA, also known as ecstasy. All of them cause an effect on the brain, modifying the activity of the neuronal systems, altering the activity or availability of the neurotransmitters or emulating their actions. The risk of dependence is related to the velocity with which these drugs induce plastic changes in the brain, very much like a learning process. Such changes underlie the patient's dependence to drugs. Therefore when a long term user quits and deprives the brain abruptly of these drugs, an abstinence syndrome is precipitated and it may be quite severe. Only for marijuana it seems to be mild, misleading people to believe this drug does not cause physical dependence. Marijuana (Cannabis sativa) is a plant which has its active principle A9-tetrahydrocannabinol (THC) in almost all its parts, i. e. the flowers, stems, seeds and leaves. It actually contains over 60 cannabinoids as well as other chemical compounds. Marijuana causes euphoria followed by relaxation and several other reinforcing effects. Among the adverse effects marijuana causes: alteration of short-term memory, slowness of reflexes, depression and anxiety, bronchitis and lung infections. Marijuana effects depend on the activation of the CB1 and CB2 receptors, distributed in the entire body. The CB1 receptor is mainly present in the brain. In medicine, A9-THC has been useful in treating symptoms caused by chemotherapy, and in treating the anorexia caused by the Acquired Immune Deficiency Syndrome. Also, an antagonist of the CB1 receptor, Rimonabant, has been used to treat morbid obesity with certain degree of success. However, despite this promising application of Rimonabant, the side effects it caused led to its withdrawal from the market in Europe, Canada and Mexico. Heroin, derived from morphine, which in turn is isolated from opium, causes euphoria and analgesia, suppresses hunger, increases energy and induces sleepiness. The adverse effects are liver and kidney diseases as well as a decrease in breathing and heart rates. This drug acts on the opioid receptors: MOR, DOR and KOR. Cocaine, derived from the coca plant (Erythroxylum coca) produces immediate rewarding effects that last between 30 to 60 min, and causes anxiety once its serum concentration drops. Due to its very short half-life, it is the most addictive of all drugs. Cocaine reduces hunger, thirst and sleep. The most used forms of cocaine are powder and crack (available as rock). The mechanism of action by which cocaine and related compounds induce their effects is the blockade of the dopamine transporter at the synapsis, leaving dopamine available for a longer time at the synapses of the motivation-reward system. Cocaine and related compounds induce blood vessel constriction, muscular spasm, chest pain, and an increase in heart rate and blood pressure, thus augmenting the risk of cardiac arrest and stroke. The methamphetamine, a synthetic stimulant, is a crystalline, odorless, bitter drug which causes a pleasant feeling and euphoria. Its action mechanism is the blockade of the dopamine transporter, same as cocaine. The effects pursued by the users of crystal methamphetamine are increased alertness, increase in physical activity and decrease in hunger. Its side effects include increase in body temperature, heart rate and blood pressure, thus augmenting the risk for stroke. Methamphetamine also triggers violent behavior, anxiety, irritability, confusion, paranoia and hallucinations. This compound has been used for medical reasons, such as in the treatment of narcolepsy and obesity. 3,4-methylenedioxymethamphetamine, MDMA or ecstasy, is a synthetic compound with stimulant and hallucinatory effects. Its action is exerted mainly on the serotonin transporter, leaving serotonin available at the synapsis for a longer time. After clearance from the bloodstream this drug causes severe depression. Ecstasy is also combined with other stimulants. All the drugs discussed here induce body changes that compromise the life of the user, or his health at the very least. Despite this fact, the highly reinforcing effects the drugs produce by over activating the motivation-rewarding system compel their repetitive use. Not all users, however, are equally vulnerable to becoming addicted or respond the same way to the use of drugs. The individual response depends, in part, on genetic factors, as we discuss in the following section. It is evident that not only environmental factors account for the vulnerability to addiction. Genetic factors also have a substantial contribution. In order to facilitate the understanding of the interaction environment-gene, we define the following concepts: gene, allele, mutation, polymorphism, heritability and epigenesis. Apparently, the genetic contribution to addiction vulnerability varies depending on the drug. For example, cocaine and opiates are much more dependant on genetic factors to trigger addiction than are nicotine, alcohol or marijuana. Mutations or polymorphisms carried by several genes might make the difference between being at high or low risk for addiction. They may also underlie the degree of response to rehabilitation treatments. Addiction, then, is a result of an interaction between environment and genes. Environmental demands make the organism modify its structure and physiology in order to cope efficiently to such demands. One crucial way to do so is by changing gene expression. Changes in gene expression may be a consequence of chemical rearrangements in the chromatin structure, which lead to transcriptional modifications that affect the expression of the proteins the genes encode. Consequently, the normal functions of such proteins in different systems are also altered. These adaptive rearrangements in the chromatin structure are called epigenesis. The epigenetic changes induced by environmental stimuli have been proved to affect the expression of several neurotransmitter receptors and trophic factors, among many other molecules crucial for the proper functioning of the Central Nervous System. Hence, these chromatin's structural changes, triggered by environmental demands, are most likely to help the subject cope with such specific demands. However, this adaptation is not free of charge, and requires a toll to be paid which is: vulnerability to addiction. Finally, one question arises: Who is the person most likely to seek a drug of abuse? Statistics have shown that those patients suffering from a psychiatric illness. This hypothesis suggests that addiction is a symptom or a disease caused by a psychiatric illness such as a personality disorder, depression or schizophrenia. Hence, at the end, drug addiction would be a co-morbid entity, generating what in Spanish we call the dual-disease. On the other hand, the self-medication hypothesis also makes sense, at least for an extensive group of patients. This hypothesis suggests that patients take drugs of abuse to relief the symptoms caused by their psychiatric pathology. The present review discusses the interaction between brain circuits, drugs and genes to generate an addict patient. We do not intend to revise each field exhaustively, but rather we intend to give the reader a general scenario on the convergence of these three worlds. Thus it may be better understood how addiction develops and how it may be treated.<hr/>En este segundo artículo sobre el tema reseñamos brevemente las drogas de abuso ilícitas. Describiremos también cómo la genética contribuye en forma importante en el desarrollo de la adicción. La marihuana (Cannabis sativa) es una de las drogas más populares entre los jóvenes. Se presenta para su consumo en dos formas: hachís, como un triturado de la planta seca y como aceite. Una vez consumida, sus efectos tardan en aparecer según la vía de administración. Por ejemplo, cuando se inhala, sus efectos aparecen en unos cuantos segundos. Después de que el principio activo de la marihuana (A9-THC) llega al cerebro y se une a sus receptores (CB1), produce euforia seguida de relajación, se perciben más intensamente los olores, los sabores y los sonidos y parece que el tiempo pasa lentamente. Su consumo, al igual que todas las drogas de abuso, tiene efectos adversos. Sin embargo, la marihuana cuenta con un potencial uso en la medicina por sus propiedades antieméticas, orexigénicas y analgésicas. La heroína es derivada de la morfina (ingrediente activo del opio, Papaver somniferum). El opio se fuma o se utiliza como un extracto disuelto en alcohol (láudano), y la heroína se aspira o fuma. Sus efectos aparecen rápidamente e incluyen euforia, aumento de la energía, supresión del hambre, analgesia y somnolencia. La heroína, así como el opio y la morfina, ejercen su efecto a través de los receptores opioides. Su consumo deteriora el hígado, los riñones, los pulmones y el corazón. La cocaína (Erythroxylum coca) es una droga estimulante altamente adictiva. Al consumirla se experimenta mejoría de la autoestima y la auto-confianza, acompañada de excitación. Estos efectos son inmediatos y duran entre 30 y 60 minutos y son consecuencia de la inhibición de la recaptura de dopamina. Adicionalmente la cocaína inhibe el apetito y el sueño. Sus efectos adversos son la contracción de los vasos sanguíneos, espasmos musculares, dolor de pecho, embolias o derrames cerebrales, aumento en la frecuencia cardiaca y muerte. La metanfetamina se sintetiza fácilmente a partir de la anfetamina (derivado de la efedrina), lo que facilita su fabricación en laboratorios clandestinos. Cuando se fuma o se inyecta por vía intravenosa produce una sensación sumamente placentera (<<rush&gt;&gt; o <<flash&gt;&gt;), que dura pocos minutos. Consumida por vía oral o inhalada produce una euforia de mayor duración. Estos efectos son consecuencia del incremento de la liberación de dopamina. Entre los efectos adversos aparecen insomnio, incremento en la actividad física (por lo cual suele ser consumida por deportistas) y disminución del apetito (este es un motivo adicional de consumo), incremento de la temperatura corporal, aumento en el ritmo cardíaco y la presión arterial. La 3,4-metilenedioximetanfetamina, MDMA o éxtasis, es estimulante y psicodélico. Produce un efecto vigorizante, distorsiona la percepción, incluida la del tiempo. Su principal efecto es inhibir el trasportador de serotonina, pero también aumenta la disponibilidad de noradrenalina y dopamina. La adicción depende de factores sociales y psicológicos, pero la contribución genética es muy importante. Nuestros genes pueden hacernos vulnerables al consumo de drogas. Algunos polimorfismos de diversos genes nos pueden volver sensibles a la adicción o incluso dificultar la eficiencia de los tratamientos orientados a la rehabilitación. Uno de los polimorfismos más estudiados es el de las enzimas hepáticas (CYP450), asociados a la vulnerabilidad para la adicción al tabaco, el alcohol y la heroína. Adicionalmente, debemos considerar que nuestro material genético responde a los estímulos ambientales (epigénesis), de tal forma que condiciones ambientales inadecuadas, v. gr. pobre cuidado maternal, puede cambiar nuestra conducta (baja respuesta al estrés) y tornarnos vulnerables a la adicción.