Allergy to ailanthus altissima pollen: a local allergen to consider

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Remittance or persistence of attention deficit-hyperactivity disorder (ADHD) and its impact on recidivism in risky driving behaviors.

OBJECTIVE: Recent data regarding the persistence or remittance of attention deficit-hyperactivity disorder (ADHD) diagnosis into adulthood raise the question of its possible role in crucial public health issues, including road safety, especially when neurocognitive capacities are challenged. METHODS: The study included 611 participants with serious traffic violations. The Spanish version of the Mini International Neuropsychiatric Interview (M.I.N.I.) was used to assess psychopathology. They were grouped into 3 diagnostic conditions: non-ADHD, persistent ADHD (ADHD-P), and remittent ADHD (ADHD-R). Several risky driving behaviors were analyzed. RESULTS: Although participants with ADHD have more driving violations relative to non-ADHD, ADHD-R, and ADHD-P drivers have similar profiles. ADHD-R and ADHD-P drivers are more prone to perform risky and recidivistic behaviors relative to non-ADHD counterparts (P = .044 and P = .047, respectively); ADHD-R and ADHD-P participants are statistically comparable in this proneness (P = .772). CONCLUSION: These results suggest that the underlying core deficits of ADHD-attention and other executive disabilities-persist despite the fact that some people no longer reach the threshold for clinical diagnosis.

Practical Guidelines for Perioperative Hypersensitivity Reactions.

Perioperative hypersensitivity reactions constitute a first-line problem for anesthesiologists and allergists. Therefore, hospitals should have a consensus protocol for the diagnosis and management of these reactions. However, this kind of protocol is not present in many hospitals, leading to problems with treatment, reporting of incidents, and subsequent etiological diagnosis. In this document, we present a systematic review of the available scientific evidence and provide general guidelines for the management of acute episodes and for referral of patients with perioperative hypersensitivity reactions to allergy units. Members of the Drug Allergy Committee of the Spanish Society of Allergy and Clinical Immunology (SEAIC) have created this document in collaboration with members of the Spanish Anesthesia Society (SEDAR). A practical algorithm is proposed for the etiologic diagnosis, and recommendations are provided for the management of hypersensitive patients.

Practical guidelines for perioperative hypersensitivity reactions

Perioperative hypersensitivity reactions constitute a first-line problem for anesthesiologists and allergists. Therefore, hospitals should have a consensus protocol for the diagnosis and management of these reactions. However, this kind of protocol is not present in many hospitals, leading to problems with treatment, reporting of incidents, and subsequent etiological diagnosis. In this document, we present a systematic review of the available scientific evidence and provide general guidelines for the management of acute episodes and for referral of patients with perioperative hypersensitivity reactions to allergy units. Members of the Drug Allergy Committee of the Spanish Society of Allergy and Clinical Immunology (SEAIC) have created this document in collaboration with members of the Spanish Anesthesia Society (SEDAR). A practical algorithm is proposed for the etiologic diagnosis, and recommendations are provided for the management of hypersensitive patients

Las reacciones de hipersensibilidad perioperatorias constituyen un problema de primera línea para los anestesiólogos y alergólogos, por lo que es recomendable que los hospitales tengan un protocolo de consenso para el diagnóstico y el tratamiento de estas reacciones. Sin embargo, este tipo de protocolos no está presente en muchos hospitales, lo que conlleva problemas en el tratamiento, la comunicación de incidentes y el posterior diagnóstico etiológico. Este documento ha sido creado por miembros del Comité de Alergia a Medicamentos de la Sociedad Española de Alergia e Inmunología Clínica (SEAIC) en colaboración con miembros de la Sociedad Española de Anestesia (SEDAR). Se ha realizado una revisión sistemática de la evidencia científica disponible y se proporcionan pautas generales para el manejo de episodios agudos y para la derivación de pacientes con reacciones de hipersensibilidad perioperatoria a los Servicios de Alergología. Se propone un algoritmo práctico para el diagnóstico etiológico y se brindan recomendaciones para el manejo de pacientes con reacciones alérgicas perioperatorias

Psychopathology and traffic violations in subjects who have lost their driving license.

BACKGROUND: The persistence of risky behaviors while driving and traffic accidents despite campaigns to increase awareness suggest that there may be underlying causes that maintain proneness to traffic violations. The aim of the current study was to assess: a) the prevalence of psychopathology in a sample of people who have lost their driving license due to former traffic violations and b) the discriminatory capacity of each psychopathological disorder to differentiate among people with high and low proneness to perform risky behaviors while driving. METHODS: 383 participants in a course to recover their driving license after its loss due to previous traffic violations were included. The International Neuropsychiatric Interview (M.I.N.I.) according to DSM-IV was used to assess psychopathology. RESULTS: Between 67% and 76.2% of the participants had been affected by a lifetime psychopathological disorder until the moment of assessment. The most prevalent diagnoses were substance abuse including alcohol (52.5-62.7%), ADHD (19.7-28.5%), depression (7.9-14.4%) and anxiety (3.6-12.4%). Substance abuse and ADHD also showed the strongest set of associations with specific risk behaviors, but ADHD emerged as the most discriminant disorder to distinguish between those people at high and low risk of while driving. CONCLUSIONS: The results of the current study suggest that addressing psychopathology explicitly to prevent risky behaviors and recidivism while driving would provide benefits in this area.

Pharmacogenetics of methylphenidate response and tolerability in attention-deficit/hyperactivity disorder.

Methylphenidate (MPH) is the most frequently used pharmacological treatment in children with attention-deficit/hyperactivity disorder. However, a considerable interindividual variability exists in clinical outcome, which may reflect underlying genetic influences. We analyzed 57 single-nucleotide polymorphisms in 9 dopamine-related candidate genes (TH, DBH, COMT, DAT1 and DRD1-5) as potential predictors of MPH efficacy and tolerability, and we considered prenatal and perinatal risk factors as environmental hazards that may influence treatment effects in a gene-by-environment analysis. Our results provide evidence for the contribution of DRD3 (P=0.041; odds ratio (OR)=4.00), DBH (P=0.032; OR=2.85), TH (P=5.5e-03; OR=4.34) and prenatal smoking (P=1.7e-03; OR=5.10) to the clinical efficacy of MPH, with a higher risk for treatment failure in genetically susceptible subjects whose mother smoked during pregnancy. Adverse events after MPH treatment were significantly associated with variation in DBH (P=6.4e-03; OR=0.28) and DRD2 (P=0.047; OR=3.76). This study suggests that the dopaminergic system together with prenatal smoking exposure may moderate MPH treatment effects.

Psychometric validation of the Spanish version of the DHRQoL questionnaire

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Hypersensitivity reactions to biological drugs.

Strictly speaking, biological drugs are defined as drugs obtained using biotechnology that act on the immune system. They encompass monoclonal antibodies, fusion proteins, and cytokines. Although they are restricted to specific diseases, they have been increasingly used in recent years, with the consequent reporting of adverse reactions, many of which occur during the postmarketing phase. Because of the characteristics of adverse reactions, a new classification has been proposed. Hypersensitivity reactions are beta-type reactions and include infusion reactions and injection site reactions. In some cases, an immune mechanism mediated by IgE, IgG, or T cells is involved. Clinical symptoms vary widely, from skin reactions to anaphylaxis. Diagnostic studies are based on skin tests and in vitro tests (specific IgE, basophil activation test). Most are not standardized and are conducted in small groups of patients, thus making it impossible to obtain sensitivity and specificity values. With some biological drugs, desensitization protocols have proven successful. In this review, we discuss hypersensitivity reactions to biological drugs and the diagnostic tests used to assess these reactions.

Hypersensitivity reactions to biological drugs

Strictly speaking, biological drugs are defined as drugs obtained using biotechnology that act on the immune system. They encompass monoclonal antibodies, fusion proteins, and cytokines. Although they are restricted to specific diseases, they have been increasingly used in recent years, with the consequent reporting of adverse reactions, many of which occur during the postmarketing phase. Because of the characteristics of adverse reactions, a new classification has been proposed. Hypersensitivity reactions are beta-type reactions and include infusion reactions and injection site reactions. In some cases, an immune mechanism mediated by IgE, IgG, or T cells is involved. Clinical symptoms vary widely, from skin reactions to anaphylaxis. Diagnostic studies are based on skin tests and in vitro tests (specific IgE, basophil activation test). Most are not standardized and are conducted in small groups of patients, thus making it impossible to obtain sensitivity and specificity values. With some biological drugs, desensitization protocols have proven successful. In this review, we discuss hypersensitivity reactions to biological drugs and the diagnostic tests used to assess these reactions (AU)

En sentido estricto se consideran fármacos biológicos aquellos fármacos obtenidos por biotecnología que actúan en el propio sistema inmune. Engloban básicamente anticuerpos monoclonales, proteínas de fusión y citocinas. Aunque su indicación está restringida a determinadas enfermedades, su uso ha ido en aumento en los últimos años y en consecuencia también la comunicación de reacciones adversas, muchas de ellas observadas post comercialización. Debido a sus características se ha propuesto una nueva clasificación para las reacciones adversas, en la que, las reacciones de hipersensibilidad corresponden a las reacciones de tipo be incluyen reacciones de infusión y reacciones localizadas en el punto de inyección del fármaco. En algunas de estas reacciones se ha demostrado la participación de un mecanismo de hipersensibilidad inmune, bien sea mediado por IgE, IgG o por células T. Los síntomas clínicos que presentan los pacientes son muy variados, desde síntomas cutáneos a anafilaxia. Los estudios diagnósticos se basan en pruebas cutáneas, y en pruebas in vitro (IgE específica, TAB). La mayoría de pruebas no están estandarizadas y están realizadas en pequeños grupos de pacientes, lo que no permite obtener valores de sensibilidad y especificidad. Con algunos de estos fármacos se han aplicado protocolos de desensibilización con buenos resultados. En este artículo se revisan las reacciones de hipersensibilidad inducidas por los fármacos biológicos así como las pruebas utilizadas para el diagnóstico (AU)

Cortisol responses in children and adults with attention deficit hyperactivity disorder (ADHD): a possible marker of inhibition deficits.

Attention deficit hyperactivity disorder (ADHD) is a heterogeneous disease whose neurobiological background is not completely understood. It has been proposed that deficits of the inhibitory function with an underactive behavioral inhibition system (BIS) may be in the core of ADHD. In this regard, this review summarizes all studies that examine the involvement of cortisol in ADHD. Differences in cortisol responses from different ADHD subtypes, hyperactive/impulsive, inattentive, and combined, are analyzed. In addition, we examine the role of comorbidities as confounding factors in the study of cortisol in ADHD, including comorbid disruptive behavioral disorder (DBD), as well as anxiety and depressive disorders. Because ADHD is a neurodevelopmental condition and approximately half of the children enter adulthood with the disorder, we review cortisol studies in adults and children separately. Two diverse patterns of cortisol have been reported both in children and adults with ADHD. Blunted cortisol responses to stress are associated with comorbid DBD, whereas high cortisol responses are associated to comorbid anxiety disorders. Nevertheless, the inhibitory deficits in ADHD do not appear to be related directly to cortisol deficits in either children or adults. This review increases our understanding of the heterogeneity of ADHD and could help in determining new strategies for the treatment of these patients. Future studies including gender and a more systematic methodology to study the cortisol response are needed.

Corticotropin releasing factor and neuroplasticity in cocaine addiction.

Corticotropin releasing factor (CRF), one of the major effectors of stress, plays a major role in the natural course of drug addiction by accelerating the acquisition of psychostimulant self-administration and increasing incentive motivation for the drug itself and for drug-associated stimuli. Stress-induced CRF is also considered a predictor of relapse and is responsible for feelings of anxiety and distress during cocaine withdrawal. Despite this knowledge, the role of CRF has not been explored in the context of recent research on reward-related learning, built on the hypothesis that neuroplastic changes in the mesocorticolimbic circuitry underlie addiction. The present review explores the effects of stress on the pattern of interaction between CRF, dopamine and glutamate in distinct structures of the mesocorticolimbic circuitry, including the ventral tegmental area (VTA), amygdala, bed nucleus of stria terminalis (BNST) and the prefrontal cortex (PFC), after acute and chronic cocaine consumption as well as in early withdrawal and protracted abstinence. A better knowledge of the neurochemical and cellular mechanisms involved in these interactions would be useful to elucidate the role of CRF in cocaine-induced neuronal plasticity, which could be useful in developing new pharmacological strategies for the treatment of cocaine addiction.

Brain magnetic resonance imaging findings in acute relapses of neuromyelitis optica spectrum disorders.

We studied cranial magnetic resonance imaging (MRI) lesions in three women with acute attacks of recurrent longitudinally extensive transverse myelitis (r-LETM), recurrent-optic neuritis (r-ON) and r-LETM-CNS. Neuromyelitis Optica -immunoglobulin (IgG) antibody was positive in all cases. Brain MRI (1.5 Tesla) was performed according to protocol from consortium MS centre. We described the cranial lesions in brain MRI of acute relapses. These lesions were different from MS, most had an asymptomatic course which disappeared with time, protocol from consortium of MS centre criteria for brain MRI and seropositivity of NMO-IgG are useful tools for differentiate acute lesions of NMO/MS.

Brain-derived neurotrophic factor and its intracellular signaling pathways in cocaine addiction.

Cocaine addiction is one of the severest health problems faced by western countries, where there is an increasing prevalence of lifelong abuse. The most challenging aspects in the treatment of cocaine addiction are craving and relapse, especially in view of the fact that, at present, there is a lack of effective pharmacological treatment for the disorder. What is required are new pharmacological approaches based on our current understanding of the neurobiological bases of drug addiction. Within the context of the behavioral and neurochemical actions of cocaine, this paper considers the contribution of brain-derived neurotrophic factor (BDNF) and its main intracellular signaling mechanisms, including mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) and phosphatidylinositol 3-kinase (PI3K), in psychostimulant addiction. Repeated cocaine administration leads to an increase in BDNF levels and enhanced activity in the intracellular pathways (PI3K and MAPK/ERK) in the reward-related brain areas, which applies especially several days following withdrawal. It has been hypothesized that these neurochemical changes contribute to the enduring synaptic plasticity that underlies sensitized responses to psychostimulants and drug-conditioned memories leading to compulsive drug use and frequent relapse after withdrawal. Nevertheless, increased BDNF levels could also have a role as a protection factor in addiction. The inhibition of the intracellular pathways, ERK and PI3K, leads to a disruption in sensitized responses and conditioned memories associated with cocaine addiction and suggests new, potential therapeutic strategies to explore in the dependence on psychostimulants.

Brain magnetic resonance imaging findings in relapsing neuromyelitis optica.

BACKGROUND: Some studies showed abnormalities in brain magnetic resonance imaging (MRI) of relapsing neuromyelitis optica (R-NMO) from 12 to 46%. These abnormalities are described as compatible/non-compatible with multiple sclerosis (MS). OBJECTIVE: To describe the abnormal brain MRI lesions in R-NMO with imaging studies conducted with more sensitive white matter change techniques. METHODS: Thirty patients with R-NMO were selected. All MRI brain studies were performed with a 1.5-T Siemens MRI system according to the Standardized MR Imaging Protocol for Multiple Sclerosis from the Consortium of MS Centers Consensus Guidelines. RESULTS: Brain MRI images were evaluated in 29 R-NMO cases because in one case the MRI images were not appropriate for the study. Of these 29 brain MRI studies, 19 cases (65.5%) had at least one or more lesions (1-57) and 10 were negative (34.4%). Brain MRI findings in 19 cases were characterized in T2/fluid-attenuated inversion-recovery (FLAIR) by the presence of subcortical/deep white matter lesions in 16 (84.2%) cases (1-50), most of them <3 mm and without juxtacortical localization. Periventricular lesions were observed in 13 (68.4%) cases, but morphologically they were not oval, ovoid or perpendicularly orientated. Infratentorial lesions, all >3 mm, were observed in 4 (21.05%) cases without cerebellar involvement. T1 studies demonstrated absence of hypointense regions. Optic nerve enhancement was observed in 6/19 patients (31.5%). None of the brain MRI abnormalities observed were compatible with Barkhof et al. criteria of MS. CONCLUSIONS: This study, based on a Cuban patient population, with long duration of disease, good sample size and detailed characterization by MRI, demonstrated the brain MRI pattern of R-NMO patients, which is different from MS.

Down's syndrome and neuromyelitis optica (Devic's disease). An autopsy-proven case.

Neuromyelitis optica (NMO) has been attributed to different underlying pathological events. The aim of this paper is to present the first case report of a patient with Down's syndrome (DS) who died of a fulminant NMO. A 29-year-old woman with DS developed acute transverse myelitis, with complete visual loss and swollen optic discs. Two days later, she developed quadriplegia, respiratory arrest and died. The anatomical study demonstrated typical findings of DS in the brain without demyelinating lesions. A severe destruction of medulla and cervical cord with a very high degree of demyelination of the optic nerves was typical of monophasic NMO (Devic's disease). Most of the cases of NMO in Cuba are of the relapsing form, but this case report is the first one with monophasic NMO and DS with a very aggressive course. The link of the pathogenetic relationship between DS and NMO remains unclear; it may well be coincidence but the fact that the patient died very shortly after the onset suggests, at least on clinical grounds, that the presence of DS could have accelerated the fatal evolution of NMO.

Sistema dopaminérgico y adicciones / The dopaminergic system and addictions

Objetivo. Todas las sustancias psicoactivas con alto potencial de abuso se caracterizan por alterar la función del sistema de neurotransmisión dopaminérgico mesocorticolímbico. En este artículo se propone realizar una revisión de los mecanismos neurobiológicos que están en la base del desarrollo del trastorno adictivo. Desarrollo. La ingesta aguda de drogas provoca un aumento de los niveles de dopamina extracelular que, en individuos vulnerables, puede significar el inicio del proceso adictivo. El consumo crónico se acompaña de una disminución de la función dopaminérgica con desarrollo de cambios neuroadaptativos en las vías mesolímbicas y mesocorticales. En el córtex prefrontal, los cambios en la función dopaminérgica pueden producir un desequilibrio entre los receptores D1 y D2, con un predominio de las funciones inhibitorias de esta estructura. La inervación dopaminérgica de la amígdala y su interacción con el núcleo accumbens desempeña un papel esencial en el condicionamiento de estímulos ambientales, capaces de desencadenar el deseo de consumo y la recaída. En pacientes dependientes, los cambios dopaminérgicos se extienden desde las regiones límbicas a las asociativas y sensoriomotoras del estriado, y afectan a los circuitos corticoestriatocorticales. Conclusión. La implicación del sistema dopaminérgico es crucial en el desarrollo de la adicción, desde las primeras fases en que el consumo de droga empieza como una conducta instrumental dirigida a un objetivo, hasta la consolidación de la adicción como hábito compulsivo, controlado por mecanismos estímulo- respuesta, que invade, progresivamente, todas las esferas de la vida del individuo

Aim. All psychoactive substances with a high abuse potential are characterized by altering the mesocorticolimbic dopaminergic neurotransmission system. In this article it is proposed to review the neurobiological mechanisms that comprise the foundation of the development of addiction. Development. The acute drug intake provokes an increase in extracellular dopamine which, in vulnerable individuals, could be the start of the addictive process. Chronic drug use is accompanied by a reduction in the dopaminergic function with the development of neuroadaptive changes in the mesolimbic and mesocortical pathways. In the prefrontal cortex, the changes in dopaminergic function produce an inbalance between receptors D1 and D2, which leads to a predominance of inhibitatory function. Dopaminergic innervation in the amygdala and its interaction with the nucleus accumbens plays an essential role in the conditioning of environmental stimuli, and can trigger the craving and relapse. In drug dependent patients, dopaminergic changes extend from the limbic regions to the associative and sensorimotor striatum, and affect the cortico-striatico-cortical circuits. Conclusion. The involvement of the dopaminergic systems is crucial in the development of addiction, from the early phases in which drug use begins as an object-directed instrumental behavior, to the consolidation of the addiction as a compulsive habit, controlled by stimulus-response mechanisms, which progressively invade all aspects of the life of an individual