Diverse cellular morphologies during lumen maturation in Anopheles gambiae larval salivary glands.

Mosquitoes are the greatest animal threat to human health, causing hundreds of millions of infections and around 1 million deaths each year. All mosquito-borne pathogens must traverse the salivary glands (SGs) to be transmitted to the next host, making this organ an ideal target for interventions. The adult SG develops from precursor cells located in the larval SG duct bud. Characterization of the larval SG has been limited. We sought to better understand larval SG architecture, secretion and gene expression. We developed an optimized method for larval SG staining and surveyed hundreds of larval stage 4 (L4) SGs using fluorescence confocal microscopy. Remarkable variation in SG cell and chromatin organization differed among individuals and across the L4 stage. Lumen formation occurred during L4 stage through secretion likely involving a coincident cellular apical lipid enrichment and extracellular vesicle-like structures. Meta-analysis of microarray data showed that larval SG gene expression is divergent from adult SGs, more similar to larval gastric cecae, but different from other larval gut compartments. This work highlights the variable cell architecture of larval Anopheles gambiae SGs and provides candidate targets for genetic strategies aiming to disrupt SGs and transmission of mosquito-borne pathogens.

Response to methylphenidate by adult and pediatric patients with attention-deficit/hyperactivity disorder: the Spanish multicenter DIHANA study.

BACKGROUND: The purpose of this multicenter Spanish study was to evaluate the response to immediate-release methylphenidate by children and adults diagnosed with attention-deficit/hyperactivity disorder (ADHD), as well as to obtain information on current therapy patterns and safety characteristics. METHODS: This multicenter, observational, retrospective, noninterventional study included 730 patients aged 4-65 years with a diagnosis of ADHD. Information was obtained based on a review of medical records for the years 2002-2006 in sequential order. RESULTS: The ADHD predominantly inattentive subtype affected 29.7% of patients, ADHD predominantly hyperactive-impulsive was found in 5.2%, and the combined subtype in 65.1%. Overall, a significant lower Clinical Global Impression (CGI) score and mean number of DSM-IV TR (Diagnostic and Statistical Manual of Mental Disorders Fourth Edition, Text Revision) symptoms by subtype were found after one year of treatment with immediate-release methylphenidate; CGI decreased from 4.51 to 1.69, symptoms of inattention from 7.90 to 4.34, symptoms of hyperactivity from 6.73 to 3.39, and combined subtype symptoms from 14.62 to 7.7. Satisfaction with immediate-release methylphenidate after one year was evaluated as "very satisfied" or "satisfied" by 86.90% of the sample; 25.75% of all patients reported at least one adverse effect. At the end of the study, 41.47% of all the patients treated with immediate-release methylphenidate were still receiving it, with a mean time of 3.80 years on therapy. CONCLUSION: Good efficacy and safety results were found for immediate-release methylphenidate in patients with ADHD.

Aditivos y trastorno del déficit de atención. Actualización / Additives and upheaval of the attention deficit. Update

En 1975 se abrió el debate sobre si el consumo de ciertos aditivos podría aumentar la hiperactividad o tener efectos perniciosos en la atención, conducta y aprendizaje, ya en población normal, ya en pacientes con trastorno por hiperactividad. Si bien los resultados han sido negativos durante decenios de investigación, desde el 2004 se ha reabierto el debate con más fuerza gracias a un nuevo metanálisis y a dos investigaciones cuyos últimos resultados se publican en septiembre del 2007. Estos artículos aportan datos positivos sobre un efecto neurobiológico leve de estos aditivos en población normal y según metanálisis también en TDA. Este efecto neurobiológico implicaría al menos un aumento de la hiperactividad. Los estudios necesitan ser replicados por otros equipos de investigadores y afinar problemas metodológicos pero por el momento cambian nuestra perspectiva sobre la influencia de estos aditivos en la hiperactividad y sobre sus efectos neurobiológicos (AU)

Artificial food colours and other food additives (AFCA) have long been suggested to affect behaviour in children.. The main putative effect of food additives is to produce overactive, impulsive, and inattentive behaviour. Despite the failure of early studies along 30 years to identify the range of proposed adverse affects, a recent meta-analysis4 of double-blinded, placebo-controlled trials and two new researches has shown a significant effect of food additives on the behaviour of children with ADHD. This effect should be to increase hyperactivity. Although these studies need to be replicated, have changed our view point about this issue (AU)

Uso de mirtazapina en el trastorno de pánico / Mirtazapine use in panic disorder

La mirtazapina es un antidepresivo con buena eficacia y pocos efectos adversos, pero también se ha señalado que ataca los síntomas de ansiedad en pacientes deprimidos. Se ha considerado que su mecanismo principal de acción para explicar esta eficacia es la mejora simultánea de la transmisión noradrenérgica y serotoninérgica. Debido a los efectos adversos que se presentan a menudo con los inhibidores selectivos de la recaptación de serotonina (ISRS) o con los antidepresivos tricíclicos (ATC) usados para tratar el trastorno de pánico, se ha usado mirtazapina en algunos estudios abiertos. Se discuten los resultados de estos estudios, principalmente los que comparan mirtazapina con los ISRS (fluoxetina, paroxetina), en cuanto a eficacia y tolerancia

Mirtazapine is an antidepressant with good efficacy and few adverse effects. This drug has also been reported to target symptoms of anxiety in depressed patients. The main mechanism for this efficacy is believed to be enhancement of both noradrenergic and serotonergic transmission. Due to the adverse effects commonly associated with the selective serotonin uptake inhibitors (SSRIs) and tetracyclic antidepressants (TCAs) used to treat panic disorder, mirtazapine has been used in some open trials. In the present article, we discuss the results of these studies, mainly those comparing mirtazapine with SSRIs (fluoxetine, paroxetine) in terms of efficacy and tolerability

Estilos y representaciones de apego en consumidores de drogas / Attachment styles and representations in drug users

El apego inseguro se ha revelado factor de riesgo de diversos problemas de salud mental. Parece plausible que el apego inseguro, en general desarrollado en la infancia, es un factor de riesgo de trastornos por consumo de drogas (TCDs), y esto podría también afectar la alianza terapéutica, y secundariamente, la evolución del TCD. Hemos revisado la literatura sobre este tema, buscando relaciones entre patrones de apego y TCDs. Los estudios publicados sobre apego y TCDs, han producido resultados poco consistentes, en parte por el uso de diferentes medidas de evaluación. Los estudios con los autoinformes de Hazan y Shaver mostraron relación sobre todo con estilo de apego evasivo. Los estudio con la Entrevista de Apego del Adulto encontraron patrones de apego devaluadores o no resueltos. Finalmente, los estudios con el modelo de Bartholomew, en consumidores de alcohol u opiáceos, han encontrado estilos preocupados o temerosos. Discusión y conclusiones: Los estudios analizados son heterogéneos en cuanto a características de la muestra que a veces incluso no se especifican (edad, tipo de droga consumida, gravedad de la adicción) y al uso de instrumentos que clasifican de modo diferente las categorías de apego. No obstante, el apego seguro es similar los TCD. También hay pocos datos que apoyen una relación entre apego preocupado o ansioso y TCDs. Si bien algunos estudios apuntan a la existencia de patrones devaluadores de apego, la mayoría de trabajos encuentran apegos evasivos o temerosos

In secure attachment has been shown to be a risk factor for a variety of mental health problems. It seems plausible that insecure attachment, usually developing during childhood, is a risk factor for substance use disorders (SUDs), and it could also have an effect on the therapeutic alliance and, accordingly, on th e SUC outcome. We have review the literature on this topic, looking for attachment patterns linked to SUDs. Published studies on attachment and SUDs have produced inconsistent results, partly due to the use os different evaluation methods. Studies working with the Hazan and Shaver self-report, showed a link mainly with avoidant attachment style. Studies using the Adult Attachment Interview found dimissing or unresolved attachment patterns. Finally, studies of alcohol and opiate users with the Bartholomew model have found preoccupied or fearful styles. Discussion and conclusions: The reviewed studies are heterogeneous in respect of the sample characteristics that are, at times, not even specified (age, kind of drugs used, severity of the addiction), and the use of instruments that classify the attachment categories in a different way. Neverthless, secure attachment is similar across all the measures and it does not seem to justify SUDs. In addition, there are few data supporting a relationship between preoccupied or anxious attachment, and SUDs. Although some studies point to the exercise of dimissing attachment patterns, the majority of studies have found avoidant or fearful attachments

[Swallowing phobia: symptoms, diagnosis and treatment]. / Fobia a tragar: clínica, diagnóstico y tratamiento.

INTRODUCTION: Choking phobia (or swallowing phobia) is characterized by a fear of swallowing foods, liquids or pills, sometimes after an episode of choking on food. METHODS: Forty-one case reports on swallowing phobia from 1978 to 2005 were studied. Clinical and therapeutic variables of the disorder were studied. RESULTS: It appears to occur more often in females (two-thirds of the cases) and has a high comorbidity with anxiety disorders (panic disorder, 41 %; obsessive conditions, 22 %, and separation anxiety, 15 %). Life-events and eating traumatic antecedents are frequently present (44% and 56% cases, respectively). Cognitive-behavioral treatments have been of proven efficacy, as well as anti-panic drugs (alprazolam, lorazepam, bromazepan, imipramine, clomipramine, fluoxetine, paroxetine) with a remission rate of 58.5%. Gender and treatment differences are also analyzed.

Fobia a tragar: clínica, diagnóstico y tratamiento / Swallowing phobia: symptoms, diagnosis and treatment

Introducción. La fobia a tragar (o a atragantarse) se caracteriza por miedo a atragantarse al ingerir comida, líquidos o pastillas, a veces tras un episodio de atragantamiento con comida. Métodos. Se han analizado las publicaciones entre 1978 y 2005 en las que se recogían 41 casos con fobia a tragar. Se estudiaron las variables clínicas y terapéuticas del trastorno. Resultados. Parece suceder más en mujeres (dos tercios de los casos) y tiene una alta comorbilidad con trastornos de ansiedad (pánico, 41 %; patología obsesiva, 22 %, y ansiedad de separación, 15 %). Con frecuencia existen antecedentes traumáticos en la ingesta o sucesos vitales (56 y 44%, respectivamente). Se han mostrado eficaces los tratamientos cognitivo- conductuales, así como fármacos antipánico (alprazolam, lorazepam, bromazepam, imipramina, clomipramina, fluoxetina, paroxetina) con una tasa de remisiones completas del 58,5 %. Estudiamos las diferencias por sexo y por tratamientos utilizados

Introduction. Choking phobia (or swallowing phobia) is characterized by a fear of swallowing foods, liquids or pills, sometimes after an episode of choking on food. Methods. Forty-one case reports on swallowing phobia from 1978 to 2005 were studied. Clinical and therapeutic variables of the disorder were studied. Results. It appears to occur more often in females (twothirds of the cases) and has a high comorbidity with anxiety disorders (panic disorder, 41 %; obsessive conditions, 22 %, and separation anxiety, 15 %). Life-events and eating traumatic antecedents are frequently present (44% and 56% cases, respectively). Cognitive-behavioral treatments have been of proven efficacy, as well as anti-panic drugs (alprazolam, lorazepam, bromazepan, imipramine, clomipramine, fluoxetine, paroxetine) with a remission rate of 58.5%. Gender and treatment differences are also analyzed

Aspectos evolucionistas de los trastornos afectivos, revisión crítica y propuesta de un nuevo modelo / Evolutionary aspects of affective disorders, critical review and proposal of a new model

La psicopatología evolucionista enfoca la psicopatología bajo el prisma de la teoría de la evolución, generando nuevas hipótesis etiológicas de los trastornos mentales. Para la psicopatología evolucionista las emociones son sistemas de respuesta o formas especiales de funcionamiento prefijados genéticamente, producto de la evolución, que nos permiten adaptarnos al ambiente, a sus amenazas y oportunidades, y que ejercen su función mediante una serie de cambios coordinados a nivel fisiológico, cognitivo y conductual. Existen varios modelos evolucionistas que intentan explicar la función adaptativa de la depresión: reacción ante la pérdida de jerarquía en la lucha social, escenificación de la sumisión o rendición, forma de lograr el cambio de motivación al no lograr un objetivo, función de búsqueda de apoyo social, paralelismos con la fase de desesperación del experimento de separación de crías de monos de sus madres, hibernación, etc.Nuestro modelo intenta explicar la depresión, los estados maníacos, hipomaníacos y otros estados afectivos. A nuestro juicio la mayoría de los trastornos afectivos son procesos patológicos (y no adaptativos) que surgen de un mecanismo desencadenante innato (MDI) que inicialmente sí es adaptativo, pero se ha alterado, y cuya función es regular el nivel de energía y actividad a partir de la intensidad y duración de luz (MDI-A). Este MDI-A desencadena respuestas vegetativas, endocrinas y conductuales presentes tanto en humanos como en animales filogenéticamente más antiguos. Más recientemente en la filogenia se han acoplado a este MDI-A otros mecanismos (MDI-AA). En el hombre los desencadenantes de los MDI-AA son de índole social y se han añadido nuevas respuestas (como el humor) a las respuestas más antiguas del MDI-A

Evolutionary psychopathology incorporates psychiatry into biology via theory of evolution, generating new etiological hypothesis for mental disorders. For evolutionary psychopathology emotions are a response system or a genetically programmed, specialized state of functioning, formed by natural selection, that allows us to adapt to the environment, increasing the ability to cope with threats and opportunities. Emotions exert their function by coordinated physiological, psychological and behavioral changes. Many functions have been suggested for low mood or depression, including communicating a need for help, signaling yielding in a hierarchy conflict, fostering disengagement for commitments to unreachable goals, regulating patterns of investment, parallelism with despair phase of separation from mother situation in monkeys, hibernation, etc. ;;Despite other evolutionary models, our model not only tries to explain depression but mania, hypomania and other affective disorders as well. For us, most affective disorders are pathological states (and not adaptive ones), due to dysfunction of an innate precipitating mechanism (IPM). IPM function is to regulate energy and activity levels according to intensity and duration of light (namely IPM-A). This IPM-A is responsible for vegetative, endocrine and behavioral responses that are present in humans and more ancient phylogenetic animals. More recently in the phylogeny, other mechanisms (IPM-AA) have coupled to this IPM-A. In the human being, the precipitating factors of IPM-AA are predominately social. IPM-AA add new responses (such as mood) to the older responses of IPM-A

[Evolutionary aspects of affective disorders, critical review and proposal of a new model]. / Aspectos evolucionistas de los trastornos afectivos, revisión crítica y propuesta de un nuevo modelo.

Evolutionary psychopathology incorporates psychiatry into biology via theory of evolution, generating new etiological hypothesis for mental disorders. For evolutionary psychopathology emotions are a response system or a genetically programmed, specialized state of functioning, formed by natural selection, that allows us to adapt to the environment, increasing the ability to cope with threats and opportunities. Emotions exert their function by coordinated physiological, psychological and behavioral changes. Many functions have been suggested for low mood or depression, including communicating a need for help, signaling yielding in a hierarchy conflict, fostering disengagement for commitments to unreachable goals, regulating patterns of investment, parallelism with despair phase of separation from mother situation in monkeys, hibernation, etc. Despite other evolutionary models, our model not only tries to explain depression but mania, hypomania and other affective disorders as well. For us, most affective disorders are pathological states (and not adaptive ones), due to dysfunction of an innate precipitating mechanism (IPM). IPM function is to regulate energy and activity levels according to intensity and duration of light (namely IPM-A). This IPM-A is responsible for vegetative, endocrine and behavioral responses that are present in humans and more ancient phylogenetic animals. More recently in the phylogeny, other mechanisms (IPM-AA) have coupled to this IPM-A. In the human being, the precipitating factors of IPM-AA are predominately social. IPM-AA add new responses (such as mood) to the older responses of IPM-A.

Violence in mental disorders and community sample: an evolutionary model related with dominance in social relationships.

The major risk determinants of violence are to be young and male, to have low socioeconomic status and suffering substance abuse. This is true whether it occurs in the context of a concurrent mental illness or not; i.e., mental disorders are neither necessary, nor sufficient causes for violence. Intense motivation is a facilitating factor for violence in clinical and non clinical samples. This explains why 'normal' people, are implicated in planned violence at higher rates than mentally ill (e.g. in criminal acts against property). However mentally ill patients are more easily implicated in impulsive violence or in violence without obvious cause due to veiled motivation fuelled by unidentified symptoms. Subjective or real awareness of competitive disadvantage increases motivation for violence (e.g. paranoid, narcissistic symptoms, etc.). Many psychiatric disorders as antisocial disorder, borderline, schizophrenia, have most of the factors that facilitate the appearance of violence. Antisocial disorder is a good model to study determinants of violence in normal samples as it is present in young males that do not have any psychotic symptom, have stable symptomatology, self control under scrutiny, and their motivations are similar to normal samples. Our evolutionary model suggests that there is a non random association of genetic factors (genes, pseudogenes, promoting areas, etc.), that is, a genetic cluster (cluster DO), whose phylogenetic function is to motivate to be the dominant in social relationships. To be the dominant is a major psychological feature present in many social groups of animals, included primates. DO cluster have sense from an evolutionary viewpoint: when expressed in no pathological way it increases inclusive fitness (transmission of the genes of a person genotype whether by oneself or by relatives reproduction). Features of cluster DO in humans are expressed differently according to sex, age, moral education, level of intelligence, etc. Cluster DO has higher phenotypical expression in males and young people. Primary antisocial personality disorder and other related disorders (cluster B personality disorders, disocial, defiant disorder, etc.), are a pathological manifestation of this cluster DO. Some other genetic clusters that causes the genetic liability to some disorders (e.g. attention deficit disorder) are non random associated with cluster DO, thus explaining clinical comorbidity. According to our model, motivation for dominance usually prevails over motivation for material benefit or antinormative behaviour, this explains some incongruent behaviour in antisocial patients not elucidated by other models. Along with the primary expressed feature of dominance of cluster DO there are other secondary features that have been identified by psychobiological studies: novelty seeking, intolerance for frustration, impulsiveness, fearless, aggressiveness, higher threshold for activation of the sympathetic system, lack of empathy, egoism, non acceptance of rules, defiant and rebellious behaviour, manipulation in social interactions, selfishness and deficits in altruism or in social co-operation.

Violencia y jerarquía en los trastornos psiquiátricos y en la comunidad. Revisión y propuesta de un modelo evolucionista / Violence and hierachy in psychiatric disorders and inthe community. Review and proposal of a evolutionary model

El objetivo principal de este artículo es determinar las relaciones entre violencia, cooperación y dominio jerárquico, estudiando los trastornos mentales y específicamente el trastorno de personalidad antisocial (TP A) desde una perspectiva evolucionista. Los principales determinantes del riesgo de violencia son biológicos (ser varón joven) y socioeconómicos (bajo nivel socioeconómico y abuso de sustancias). Esto es cierto tanto si ocurre en el contexto de una enfermedad mental o no, es decir, los trastornos mentales no son causas suficientes ni necesarias para la violencia. Nuestro modelo evolucionista sugiere que hay un grupo de genes (cluster DO) cuya función filogenética es motivar para ser el dominante en las relaciones sociales. Este cluster DO tiene mayor expresión fenotípica en hombres y en jóvenes. Los rasgos que expresa son: búsqueda de novedades, intolerancia a la frustración, impulsividad, osadía, agresividad, mayor umbral para la activación de sistema simpático, falta de empatía, egoísmo, rebeldía, no aceptación de reglas, manipulación en las interacciones sociales y déficits en altruismo o en la cooperación social. Estos rasgos se expresan de modo diferente según el sexo, la edad, la educación moral, el nivel de inteligencia, etc. El Trastorno antisocial de la personalidad, en sus diversas formas, es una manifestación patológica de este cluster DO

The major risk determinants of violence are biological (predominantly age, namely to be young, and sex, namely to be male) and socio-economic (namely a low status and substance abuse). This is true whether it occurs in fue context of a concurrent mental illness or not; i.e., mental disorders are neither necessary, nor sufficient causes for violence. Antisocial disorder appears mainly in young male and is a good model for studying violence in normal population. Our evolutionary model suggests that there is a cluster of genes (cluster DO) whose phylogenetic function is to motivate to be fue dominant in social relationships. Cluster DO has higher phenotypical expression in males and young people. There are other features that expressed by cluster DO are novelty seeking, intolerance to frustration, impulsiveness, fearless, aggressiveness, higher threshold for activation of fue sympathetic system, lack of empathy, egoism, non acceptance of roles (being rebellious), manipulation in social interactions, egoism and deficits in altruism or in social co-operation. Features of cluster DO are expressed differentially according to sex, age, moral education, level of intelligence, etc. Antisocial personality disorder, in their diverse forms, are a pathological manifestation of this cluster DO

[Treatment of Tourette syndrome and its comorbidity: experience with 17 cases]. / Tratamiento del síndrome de Tourette y su comorbilidad: presentación de 17 casos.

INTRODUCTION: Clinical characteristics and comorbid disorders of Tourette syndrome (TS) are reviewed along with a presentation of our experience with 17 cases. MATERIAL AND METHODS: We carried out a retrospective study of pediatric patients with TS admitted from 1998 to 2004 in Fundación Hospital Alcorcón. RESULTS: Seventeen patients were obtained, 16 of whom were men and there was only 1 woman. Present age ranged from 7 to 17 years old. Most frequent comorbid disorders were attention deficit disorder (ADD) in 9 patients, (53%), obsessive-compulsive disorder in 8 (48%) and anxiety in 7 (41%). Learning disorders were found in 7 patients (41%), 5 of whom have concurrent ADD and 1 severe obsessive compulsive disorder. Psychopharmacological treatment was withdrew in the 2 cases treated with halloperidol due to the presence of severe extrapyramidal symptoms (EPS) and in 3 of the 7 cases treated with pimozide (one of them was withdrawn due to EPS). No EPS was found with atypical neuroleptics, but sedation and weight gain was common. Methylphenidate was administered to 7 patients without an increase in tics. CONCLUSIONS: In our sample the most common comorbid disorders were ADD, obsessive-compulsive disorders, anxiety and learning disorders. Atypical neuroleptics were better tolerated than classic ones, although the incidence of side effects is elevated. Methylphenidate was not associated with tic worsening.

El uso de los nuevos antipsicóticos atípicos en el síndrome de Gilles de la Tourette / Use of atypical antipsychotics in Tourette´s syndrome

El síndrome de GiIles de la Tourette (SGT) es un trastorno neuropsiquiátrico con tics motores y vocales crónicos y una elevada comorbilidad y síntomas secundarios. Se han venido usando agonistas alfa-2 (clonidina) o antipsicóticos clásicos (haloperidol, pimocida) con buena eficacia pero mala tolerancia (Efectos adversos). Revisamos la literatura existente sobre eficacia y tolerancia de los nuevos antipsicóticos (clozapina, risperidona, olanzapina, quetiapina, amisulpride, ziprasidona) en esta patología

Tourette's syndrome is a neuropsychiatric disorder characterized by chronic motor and vocal tics and a high comorbidity and associated symptoms. Usually, alpha-2 agonists (clonidine) or typical antipsychotics (haloperidol, pimozide) have been used with a good efficacy but they are poorly tolerated (adverse effects). We review here the existing evidences on efficacy and tolerance for the new antipsychotics (clozapine, risperidone, olanzapine, quetiapine, amisulpride, ziprasidoné) on this disorder

Cólicos neonatales y psicopatología: ¿existe una relación? / Colic the newborn and psychopathology: is there a relationship?

El objetivo de esta revisión es aclarar el concepto de cólico neonatal e investigar si este llanto excesivo se asocia con un riesgo mayor de hiperactividad o problemas de conducta en la vida posterior. Asimismo se discuten la persistencia de problemas en la interacción paterno-filial, o familiar, y sus implicaciones

The purpose of this review is to clarify the concept of infantile colic and to investigate if this excessive crying is associated with an increased risk for hyperactivity or behaviour problems in later life. Persistence and implications of parent-infant, or family interaction problems are also discussed

Presentación clínica, comorbilidad y tratamiento habitual del síndrome de Gilles de la Tourette: estudio de 17 casos / Clinical presentation, comorbídíty and usual treatment of Gilles de la Tourette's syndrome: study of 17 cases

Introducción: El síndrome de Gilles de la Tourette (SGT) es un trastorno neuropsiquiátrico de inicio infantil caracterizado por tics vocales y motores múltiples y crónicos. Es frecuente la comorbilidad con trastornos psiquiátricos, sobre todo trastorno de déficit de atención con hiperactividad (TDAH), trastornos de ansiedad y trastorno obsesivo-compulsivo (TOC). Metodología: Estudiamos de modo retrospectivo 17 pacientes en edad pediátrica atendidos en consulta externa neuropediátrica o psiquiátrica, entre 1998 y 2003. Se estudiaron las variables: edad, sexo, síntomas clínicos, edad de inicio, antecedentes familiares, comorbilidad, tratamiento recibido y datos de evolución. Resultados: Todos los casos menos uno eran varones, de edad media 10 años pero edad media de inicio 5 años y 9 meses. Había comorbilidad en 82,3% de pacientes (TDAH 53%, trastornos de ansiedad 41,1 %, patología TOC 58,7%). Había antecedentes familiares en 72% de casos: 41,1 % tics y 17,6% patologías TOC. Los tratamientos más prescritos fueron antipsicóticos (n=15) y metilfenidato (n=7). El tratamiento con metilfenidato no aumentó los tics. Hubo efectos adversos en 16 pacientes, conduciendo a abandonar haloperidol (n=2) o pimocida (3 de los 7 casos) por efectos secundarios neurológicos o cardiacos. Risperidona y olanza pina produjeron aumento de peso y somnolencia pero fueron mejor tolerados. La tasa de remisión completa fue 64,7%. Conclusión: el tratamiento de SGT debería considerarse en los casos graves fijándonos también en trastornos comórbidos

Background: Tourette's syndrome (TS) is a childhood-onset neuropsychiatric disorder characterized by chronic multiple motor and vocal tics. Comorbid psychiatric disorders, particularly attention deficit hyperactivity disorder (ADHD), anxiety disorders and obsessive compulsive disorder (OCD) often are present. Methods: Seventeen pediatric cases attending an outpatient neuropediatric or psychiatric clinic from 1998 to 2003 and suffering from Tourette's disorder are retrospectively studied. Age, sex, clinical symptoms, age of onset, family history, comorbidity, treatment strategies and outcome data are described. Results: All but one case were male; mean age was 10 years but mean age of onset was 5 years and 9 months. Comorbidity was present in 82,3% of patients (ADHD 53%, anxiety disorders 41,1%, OCD spectrum 58,7%). Family history was positive in 72% of cases: 41,1% for tics and 17,6% for OC conditions. Treatments mostly prescribed were antipsychotics (n=15), and meti1phenidate (n=7). Treatment with meti1phenidate did not exacerbate tics. Adverse effects were present in 16 patients, allowing to withdraw ha1operido1 (n=2) or pimocide (3 out of 7 cases) because of neuro1ogic y/o heart side effects. Risperidone and o1anzapine produced weight gain and somno1ence but were better to1erated. The rate of total remission was 64,7%. Conclusion: treatment of TS should be considered in severe cases, focusing also on comorbid disorders

Tratamiento del síndrome de Tourette y su comorbilidad: presentación de 17 casos / Treatment of Tourette syndrome and its comorbidity: experience with 17 cases

Introducción. Presentamos las características clínicas y trastornos comórbidos asociados y evaluamos los resultados de los tratamientos farmacológicos empleados en 17 pacientes con síndrome de Tourette (ST). Material y métodos. Revisión retrospectiva de los pacientes pediátricos diagnosticados de ST en nuestro hospital entre 1998 y 2004. Resultados. De los 17 pacientes, 16 son varones y sólo 1 mujer, con edades actuales comprendidas entre 7 y 17 años. Los trastornos comórbidos más frecuentes fueron el trastorno por deficit de atención con hiperactividad (TDAH) en 9 pacientes (53 Ofo), conductas obsesivo-compulsivas en 8 (48 %) Y ansiedad en 7 (41 %). Presentaban problemas de aprendizaje 7 (41 %), de los cuales 5 asociaban un TDAH y 1 un trastorno obsesivo-compulsivo (TOC) severo. Encontramos efectos farmacológicos adversos severos que obligaron a la retirada de la medicación en los 2 casos tratados con haloperidol (ambos de tipo extrapiramidal) y en 3 de los 7 (43 %) de los tratados con pimozida (1 de ellos de tipo extrapiramidal). No ocurrieron efectos extrapiramidales con los neurolépticos atípicos, pero fueron frecuentes la sedación y el aumento de peso. Siete pacientes fueron tratados con metilfenidato, sin empeoramiento de los tics. Conclusiones. En nuestra serie los trastornos comórbidos más frecuentes fueron el TDAH, conductas obsesivo-compulsivas, ansiedad y dificultades en el aprendizaje. Los neurolépticos atípicos fueron mejor tolerados que los clásicos, aunque la incidencia de efectos adversos es también elevada. El metilfenidato no se ha asociado a empeoramiento de los tics

Introduction. Clinical characteristics and comorbid disorders of Tourette syndrome (TS) are reviewed along with a presentation of our experience with 17 cases. Material and methods. We carried out a retrospective study of pediatric patients with TS admitted from 1998 to 2004 in Fundación Hospital Alcorcón. Results. Seventeen patients were obtained, 16 of whom were men and there was only 1 woman. Present age ranged fram 7 to 17 years old. Most frequent comorbid disorders were attention deficit disorder (ADD) in 9 patients, (53 %), obsessive-compulsive disorder in 8 (48 %) and anxiety in 7 (41 %). Learning disorders were found in 7 patients (41 %), 5 of whom have concurrent ADD and 1 severe obsessive compulsive disorder. Psychopharmacological treatment was withdrew in the 2 cases treated with halloperidol due to the presence of severe extrapyramidal symptoms (EPS) and in 3 of the 7 cases treated with pimozide (one of them was withdrawn due to EPS). No EPS was found with atypical neuraleptics, but sedation and weight gain was common. Methylphenidate was administered to 7 patients without an increase in tics. Conclusions. In our sample the most common comorbid disorders were ADD, obsessive-compulsive disorders, anxiety and learning disorders. Atypical neuroleptics were better tolerated than classic ones, although the incidence of side effects is elevated. Methylphenidate was not associated with tic worsening

Fobia a tragar: presentación clínica de una serie de nueve casos / Chocking phobia: clinical presentation of nines cases

Introducción: La fobia a tragar es un miedo a tragar sólidos y/o líquidos que suele responder a tratamiento conductual. Metodología: estudiamos nueve casos de fobia a tragar tratados ambulatoriamente. Se describen edad, sexo, historia familiar, comorbilidad, y datos sobre tratamiento y evolución, entre otros. Resultados: un 55% eran mujeres, edad media 25 años. El 33% tenía antecedentes familiares psiquiátricos,88% tenía comorbilidad con trastorno de pánico, patología obsesivo-compulsiva o personalidad evitativa. Los tratamientos eficaces fueron terapia cognitivo-conductual (n = 9), clomipramina (n = 2), paroxetina (n = 2) y benzodiacepinas (n = 5). Conclusión: la fobia a tragar tiene una alta comorbilidad con trastornos ansiosos, lo que condiciona el abordaje terapéutico

Introduction: Choking (swallowing) phobia is a fear of swallowing food and/or fluids that usually respondsto behaviour therapy.Methods: Nine cases attending an out patient clinic and suffering from choking phobia are retrospectively studied. Age, sex, family history, comorbidity, treatment strategies and outcome data are described. Results: Fifty-five percent of patients were female, mean age 25 years. A total of 33% had psychiatric family history, 88% had comorbidity with panic disorder, obsessive-compulsive disease or avoidant personality. Effective treatments were cognitive-behavioural therapy (n = 9), clomipramine (n = 2), paroxetine (n = 2) and benzodiazepines (n = 5). Conclusion: Swallowing (choking) phobia has a high comorbidity rate with anxious disorders, suggesting certain treatment strategies

Fobia a atragantarse en la infancia y adolescencia / Choking phobia in childhood and adolescence

Introducción: La fobia a tragar (o a atragantarse) se caracteriza por miedo a atragantarse al ingerir comida, líquidos o pastillas, a veces tras un episodio de atragantarniento con comida. Pretendemos describir las características de esta fobia en niños y adolescentes y compararlas con las que presenta en adultos. Se han analizado las publicaciones entre 1978 y 2005 en las que se recogían 13 casos con fobia a tragar en niños y adolescentes y 28 casos en adultos. Se estudiaron las variables clínicas y terapéuticas del trastorno. Resultados: En el grupo de niños y adolescentes, hubo un 53,8% de mujeres; la edad media fue 1l,23:t2,3l años (rango 8-15 años). Hubo antecedentes de atragantamiento en 53,8% de casos y problemas previos con alimentación en 23% casos y se identificaron sucesos vitales estresantes en 30,7% de casos. El tiempo hasta acudir a consulta era de 14,43:t27,86 meses. Existía comorbilidad en 76,85% de casos, sobre todo con ansiedad de separación (38,4%), pánico (23%), trastornos depresivos u obsesivos (15,4% cada uno). Recibieron tratamiento cognitivo-conductual el 100% de casos, solo (61,54%) o asociado a fármacos (imiprarnina, clomipramina, fluoxetina, paroxetina) y tardaron en mejorar 3,85+-1,86 meses. El porcentaje de casos con remisión completa fue 30,77%. Diferencias por edad: en el grupo de adultos, había mayor porcentaje de mujeres, el inicio de la fobia se asociaba a veces a enfermedad física o suceso durante la ingesta, el tiempo hasta acudir a consulta era mayor y tenía mayor comorbilidad con trastorno de pánico, un 39,28% se trató sólo con fármacos, y el porcentaje de sujetos con remisión completa fue mayor (71,43%). Discusión: la fobia a tragar presenta un perfil clínico diferente en niños o adolescentes, y adultos

Background: Choking phobia (or swallowing phobia) is characterized by a fear of swallowing foods, liquids or pills, sometimes after an episode of choking on food. We pretend to describe the characteristics of this phobia in children and adolescents and to compare them to tose presented in adult cases. Methods: Thirteen child and adolescent and twenty-eight case reports on swallowing phobia from 1978 to 2005 were studied. Results: Child and adolescent group: there was 53.8% of females, mean age was 11.23:t2.3l years (range 8-15 years). There were previous choking in 53.8% of cases and previous eating problems in 30.7% of cases. Time delay to consultation was l4.43:t27.86 months. Comorbidity appeared in 76.85% of cases, mainly separation anxiety (38.4%), panic disorder (23%) or depressive or obsessive conditions (15.4% each). A hundred percent of cases received cognitive-behavioural treatment, alone (61.54%) or combined to drugs (imipramine, c10mipramine, fluoxetine, paroxetine) and time to improval was 3.85:t1.86 months. Complete remission appeared in 30.77% of cases. Age differences: in the adult group, there was a higher female ratio, phobia onset was associated sometimes to organic disease or an event during eating, time delay to consultation was higher and there was a higher comorbidity with panic disorder; a 39.28 percent of cases was treated only with drugs and proportion of cases reaching complete remission was higher (71.43%). Discussion: choking phobia has a differential c1inical profile in children/adolescents and in adults

Mirtazapine versus paroxetine in panic disorder: an open study.

Introduction Open studies suggest that mirtazapine has efficacy in panic disorder treatment. We designed an open study that evaluates changes induced by mirtazapine compared with paroxetine in panic disorder. Methodology Patients 18-65 years old consecutively referred to a psychiatry liaison service with panic disorder (DSM-IV criteria) were offered either mirtazapine or paroxetine treatment. Results There were statistically significant reductions from baseline to week 3 and from week 3 to 8 for mirtazapine and paroxetine groups for: number of panic attacks, Beck Anxiety or Depression Inventory (BAI, BDI) Clinical Global Impresion (CGI) of panic disorder severity and CGI of panic disorder response (these variables were evaluated by the patient, the clinician or a blind evaluator). Responders at week 3 (BAI decrease of 50%) were 83% for the mirtazapine group and 84% for the paroxetine group. Responders at week 8 (number of panic attacks equal to 0) were 77% for the mirtazapine group and 73% for the paroxetine group Statistically significant differences between mirtazapine and paroxetine were found for number of panic attacks at weeks 3 and 8 and BAI at week 3, suggesting a faster response for mirtazapine. Responders at week 8 maintained a no recurrence figure of 95% at follow-up 6 months later. Panic disorder either with or without comorbid depression improved in both groups of treatment. Discussion Our study supports the hypothesis that mirtazapine has efficacy in the treatment of panic disorder either with or without comorbid depression.