Unilateral lesion of the suprachiasmatic nucleus impairs estradiol feedback, follicular development, estrous cycle and ovulation.

In brief: The SCN regulates ovulation by stimulating the preovulatory surge of gonadotropins. This study revealed an additional role in the sensitization of the hypothalamus to estradiol that changes along the estrous cycle and the side of the nucleus. Abstract: Ovulation is timed by neural signals originating at the suprachiasmatic nucleus (SCN) that trigger ovulation when converge with high estradiol levels, which indicates the maturation of ovarian follicles. We have shown that the hypothalamic regulation of ovulation is asymmetrical and we hypothesized that the paired SCN could contribute to such symmetries. We unilaterally lesioned the SCN of rats at each stage of the estrous cycle and evaluated the acute effects on the progression of their estrous cycle, follicular development and ovulation. Lesions prevented progression of the estrous cycle when performed in estrus/metestrus but not in diestrus/proestrus. Abnormalities in follicular development were observed in the nonovulating lesioned rats and this was independent of the side of the SCN destroyed and the stage of the cycle when surgery was performed. Groups of lesioned rats were then hormonally primed with GnRH or estradiol to assess the neuroendocrine pathway altered by the treatment. GnRH restored ovulation, suggesting that both SCN are needed for proper triggering of the preovulatory surge of GnRH and that unilateral lesion does not impair the sensitivity of the pituitary or the ovary to GnRH and gonadotropins, respectively. With regard to restoring ovulation, estradiol was asymmetrically effective in rats lesioned in estrous, partially effective in rats operated at diestrus and ineffective in rats at metestrus. Our results indicate that the SCN regulates the activity of the hypothalamic-pituitary-ovarian axis not only by modulating the preovulatory surge of GnRH/gonadotropins but also by promoting the hypothalamic integration of estrogenic signals from the ovaries in an asymmetric and stage-dependent fashion.

Disability Caused by Cleft Lip and Palate: A Systematic Review and Critical Valuation Appraisal.

OBJECTIVE: Measuring disability as a concept of impaired global function enables beneficiaries of treatment, the impact of treatment, and targets of health system investment to be rigorously assessed. Measures of disability are not well established for cleft lip and palate. This study aims to systematically review disability weight (DW) studies pertaining to orofacial clefts (OFCs) and identify methodological strengths and shortcomings of each approach. DESIGN: Systematic literature review of studies that met the following criteria: (1) peer-reviewed publication, (2) focus on disability valuation, (3) mention orofacial clefts, and (4) publication January 2001-December 2021. SETTING: None. PATIENTS/PARTICIPANTS: None. INTERVENTIONS: None. MAIN OUTCOME MEASURE(S): Disability weight method of valuation and the value itself. RESULTS: The final search strategy yielded 1,067 studies. Seven manuscripts were ultimately included for data extraction. The disability weights used in our studies, including those newly generated or taken from the Global Burden of Disease Studies (GBD), ranged widely for isolated cleft lip (0.0-0.100) and cleft palate with or without cleft lip (0.0-0.269). The GBD studies limited their consideration of cleft sequelae informing disability weights to impact on appearance and speech-related concerns, while other studies accounted for comorbidities such as pain and social stigma. CONCLUSIONS: Current measures of cleft disability are sparse, inadequately reflect the comprehensive impact of an OFC on function and socialization, and are limited in detail or supporting evidence. Use of a comprehensive health state description in evaluating disability weights offers a realistic means of accurately representing the diverse sequelae of an OFC.

Design, Synthesis and Preclinical Assessment of 99mTc-iFAP for In Vivo Fibroblast Activation Protein (FAP) Imaging.

Fibroblast activation protein (FAP) is expressed in the microenvironment of most human epithelial tumors. 68Ga-labeled FAP inhibitors based on the cyanopyrrolidine structure (FAPI) are currently used for the detection of the tumor microenvironment by PET imaging. This research aimed to design, synthesize and preclinically evaluate a new FAP inhibitor radiopharmaceutical based on the 99mTc-((R)-1-((6-hydrazinylnicotinoyl)-D-alanyl) pyrrolidin-2-yl) boronic acid (99mTc-iFAP) structure for SPECT imaging. Molecular docking for affinity calculations was performed using the AutoDock software. The chemical synthesis was based on a series of coupling reactions of 6-hidrazinylnicotinic acid (HYNIC) and D-alanine to a boronic acid derivative. The iFAP was prepared as a lyophilized formulation based on EDDA/SnCl2 for labeling with 99mTc. The radiochemical purity (R.P.) was verified via ITLC-SG and reversed-phase radio-HPLC. The stability in human serum was evaluated by size-exclusion HPLC. In vitro cell uptake was assessed using N30 stromal endometrial cells (FAP positive) and human fibroblasts (FAP negative). Biodistribution and tumor uptake were determined in Hep-G2 tumor-bearing nude mice, from which images were acquired using a micro-SPECT/CT. The iFAP ligand (Ki = 0.536 nm, AutoDock affinity), characterized by UV-Vis, FT-IR, 1H-NMR and UPLC-mass spectroscopies, was synthesized with a chemical purity of 92%. The 99mTc-iFAP was obtained with a R.P. >98%. In vitro and in vivo studies indicated high radiotracer stability in human serum (>95% at 24 h), specific recognition for FAP, high tumor uptake (7.05 ± 1.13% ID/g at 30 min) and fast kidney elimination. The results found in this research justify additional dosimetric and clinical studies to establish the sensitivity and specificity of the 99mTc-iFAP.

Dementia associated with disorders of the basal ganglia.

Dementia is now the leading cause of death in the United Kingdom, accounting for over 12% of all deaths and is the fifth most common cause of death worldwide. As treatments for heart disease and cancers improve and the population ages, the number of sufferers will only increase, with the chance of developing dementia doubling every 5 years after the age of 65. Finding an effective treatment is ever more critical to avert this pandemic health (and economic) crisis. To date, most dementia-related research has focused on the cortex and the hippocampus; however, with dementia becoming more fully recognized as aspects of diseases historically categorized as motor disorders (e.g., Parkinson's and Huntington's diseases), the role of the basal ganglia in dementia is coming to the fore. Conversely, it is highly likely that neuronal pathways in these structures traditionally considered as spared in Alzheimer's disease are also affected, particularly in later stages of the disease. In this review, we examine some of the limited evidence linking the basal ganglia to dementia.

Systemic scleroderma: Review and updated approach and case description to addressing pulmonary arterial hypertension and idiopathic pulmonary fibrosis: A dual challenge in treatment.

Pulmonary arterial hypertension (PAH), idiopathic pulmonary fibrosis (IPF), and scleroderma (SSc) are three interrelated medical conditions that can result in significant morbidity and mortality. Pulmonary hypertension, a condition marked by high blood pressure in the lungs, can lead to heart failure and other complications. Idiopathic pulmonary fibrosis, a progressive lung disease characterised by scarring of lung tissue, can cause breathing difficulties and impaired oxygenation. Scleroderma, an autoimmune disease, can induce thickening and hardening of the skin and internal organs, including the lungs, leading to pulmonary fibrosis and hypertension. Currently, there is no cure for any of these conditions. However, early detection and proper management can improve the quality of life and prognosis of a patient. This review focusses on PH and IPF in patients with SSc, providing information on the causes, symptoms, and treatment of these conditions, together with illustrative images. It also provides an overview of interrelated medical conditions: PH, IPF, and SSc. It emphasises the importance of early detection and proper management to improve patient quality of life and prognosis.

68Ga-DOTA-D-Alanine-BoroPro Radiotracer for Imaging of the Fibroblast Activation Protein in Malignant and Non-Malignant Diseases.

Recently, we reported a new fibroblast activation protein (FAP) inhibitor radiopharmaceutical based on the 99mTc-((R)-1-((6-hydrazinylnicotinoyl)-D-alanyl) pyrrolidin-2-yl) boronic acid (99mTc-HYNIC-D-Alanine-BoroPro)(99mTc-HYNIC-iFAP) structure for tumor microenvironment SPECT imaging. This research aimed to synthesize 68Ga-[2,2',2″,2‴-(2-(4-(2-(5-(((S)-1-((S)-2-boronopyrrolidin-1-yl)-1-oxopropan-2-yl)carbamoyl)pyridin-2-yl)hydrazine-1-carbothioamido)benzyl)-1,4,7,10-tetraazacyclododecane-1,4,7,10-tetrayl)tetraacetic acid] (68Ga-DOTA-D-Alanine-BoroPro)(68Ga-iFAP) as a novel radiotracer for PET imaging and evaluate its usefulness for FAP expression in malignant and non-malignant tissues. The coupling of p-SCN-benzene DOTA with HYNIC-iFAP was used for the chemical synthesis and further labeling with 68Ga. Radiochemical purity was verified by radio-HPLC. The specificity of 68Ga-iFAP was evaluated in HCT116 cells, in which FAP expression was verified by immunofluorescence and Western blot. Biodistribution and biokinetic studies were performed in murine models. 68Ga-iFAP uptake at the myocardial level was assessed in mice with induced infarction. First-in-human images of 68Ga-iFAP in healthy subjects and patients with myocardial infarction, glioblastoma, prostate cancer, and breast cancer were also obtained. DOTA-D-Alanine BoroPro was prepared with a chemical purity of 98% and was characterized by UPLC mass spectroscopy, FT-IR, and UV-vis. The 68Ga-iFAP was obtained with a radiochemical purity of >95%. In vitro and in vivo studies demonstrated 68Ga-iFAP-specific recognition for FAP, rapid renal elimination, and adequate visualization of the glioblastoma, breast tumor, prostate cancer, and myocardial infarction sites. The results of this research justify further dosimetry and clinical trials to establish the specificity and sensitivity of 68Ga-iFAP PET for FAP expression imaging.

Targeted Endoradiotherapy with Lu2O3-iPSMA/-iFAP Nanoparticles Activated by Neutron Irradiation: Preclinical Evaluation and First Patient Image.

Prostate-specific membrane antigen (PSMA) is expressed in a variety of cancer cells, while the fibroblast activation protein (FAP) is expressed in the microenvironment of tumors. Previously, we reported the ability of iPSMA and iFAP ligands to specifically target PSMA and FAP proteins, as well as the preparation of stable 177Lu2O3 nanoparticles (<100 nm) functionalized with target-specific peptides. This research aimed to evaluate the dosimetry and therapeutic response of Lu2O3-iPSMA and Lu2O3-iFAP nanoparticles activated by neutron irradiation to demonstrate their potential for theranostic applications in nuclear medicine. The biokinetic behavior, radiation absorbed dose, and metabolic activity ([18F]FDG/micro-PET, SUV) in preclinical tumor tissues (athymic mice), following treatment with 177Lu2O3-iPSMA, 177Lu2O3-iFAP or 177Lu2O3 nanoparticles, were assessed. One patient with multiple colorectal liver metastases (PSMA-positive) received 177Lu2O3-iPSMA under a "compassionate use" protocol. Results indicated no significant difference (p < 0.05) between 177Lu2O3-iPSMA and 177Lu2O3-iFAP, regarding tumor radiation absorbed doses (105 ± 14 Gy, 99 ± 12 Gy and 58 ± 7 Gy for 177Lu2O3-iPSMA, 177Lu2O3-iFAP, and 177Lu2O3, respectively) and tumor metabolic activity (SUV of 0.421 ± 0.092, 0.375 ± 0.104 and 1.821 ± 0.891 for 177Lu2O3-iPSMA, 177Lu2O3-iFAP, and 177Lu2O3, respectively) in mice after treatment, which correlated with the observed therapeutic response. 177Lu2O3-iPSMA and 177Lu2O3-iFAP significantly inhibited tumor progression, due to the prolonged tumor retention and a combination of 177Lu radiotherapy and iPSMA or iFAP molecular recognition. There were negligible uptake values in non-target tissues and no evidence of liver and renal toxicity. The doses received by the patient's liver metastases (42−210 Gy) demonstrated the potential of 177Lu2O3-iPSMA for treating colorectal liver metastases.

Knock-in models related to Alzheimer's disease: synaptic transmission, plaques and the role of microglia.

BACKGROUND: Microglia are active modulators of Alzheimer's disease but their role in relation to amyloid plaques and synaptic changes due to rising amyloid beta is unclear. We add novel findings concerning these relationships and investigate which of our previously reported results from transgenic mice can be validated in knock-in mice, in which overexpression and other artefacts of transgenic technology are avoided. METHODS: AppNL-F and AppNL-G-F knock-in mice expressing humanised amyloid beta with mutations in App that cause familial Alzheimer's disease were compared to wild type mice throughout life. In vitro approaches were used to understand microglial alterations at the genetic and protein levels and synaptic function and plasticity in CA1 hippocampal neurones, each in relationship to both age and stage of amyloid beta pathology. The contribution of microglia to neuronal function was further investigated by ablating microglia with CSF1R inhibitor PLX5622. RESULTS: Both App knock-in lines showed increased glutamate release probability prior to detection of plaques. Consistent with results in transgenic mice, this persisted throughout life in AppNL-F mice but was not evident in AppNL-G-F with sparse plaques. Unlike transgenic mice, loss of spontaneous excitatory activity only occurred at the latest stages, while no change could be detected in spontaneous inhibitory synaptic transmission or magnitude of long-term potentiation. Also, in contrast to transgenic mice, the microglial response in both App knock-in lines was delayed until a moderate plaque load developed. Surviving PLX5266-depleted microglia tended to be CD68-positive. Partial microglial ablation led to aged but not young wild type animals mimicking the increased glutamate release probability in App knock-ins and exacerbated the App knock-in phenotype. Complete ablation was less effective in altering synaptic function, while neither treatment altered plaque load. CONCLUSIONS: Increased glutamate release probability is similar across knock-in and transgenic mouse models of Alzheimer's disease, likely reflecting acute physiological effects of soluble amyloid beta. Microglia respond later to increased amyloid beta levels by proliferating and upregulating Cd68 and Trem2. Partial depletion of microglia suggests that, in wild type mice, alteration of surviving phagocytic microglia, rather than microglial loss, drives age-dependent effects on glutamate release that become exacerbated in Alzheimer's disease.

Preparation and Dosimetry Assessment of 166Dy2O3/166Ho2O3-iPSMA Nanoparticles for Targeted Hepatocarcinoma Radiotherapy.

This research aimed to prepare 166Dy2O3-iPSMA/166Ho2O3-iPSMA nanoparticles (166Dy2O3/166Ho2O3-iPSMA NPs) and assess the radiation absorbed dose produced by the nanosystem to hepatic cancer cells by using experimental in vitro and in vivo biokinetic data. Dy2O3NPs were synthesized and functionalized with the prostate-specific membrane antigen inhibitor peptide (iPSMA). Fourier transform infrared (FTIR) spectroscopy, transmission electron microscope (TEM), dynamic light scattering (DSL) and zeta potential analyses indicated the formation of Dy2O3-iPSMA NPs (46.11 ± 13.24 nm). After neutron activation, a stable 166Dy2O3/166Ho2O3- iPSMA nanosystem was obtained, which showed adequate affinity to the PSMA receptor in HepG2 cancer cells (Kd = 9.87 ± 2.27 nM). in vitro studies indicated high 166Dy2O3/166Ho2O3-iPSMA internalization in cancer cells, with high radiation doses to cell nuclei (107 Gy) and cytotoxic effects, resulting in a significant reduction in HepG2 cell viability (decreasing to 2.12 ± 0.31%). After intratumoral administration in mice, the nanosystem biokinetic profile indicated significant retention into the tumoral mass, producing ablative radiation doses (>70 Gy).

Impacto de los trastornos hipertensivos, la diabetes y la obesidad materna sobre el peso, la edad gestacional al nacer y la mortalidad neonatal / Impact on neonatal mortality, birth weight and gestational age, hypertensive disorders, diabetes and obesity in pregnancy

Antecedentes: Los trastornos hipertensivos, la diabetes y la obesidad en el embarazo, afectan el peso, la edad gestacional al nacer y la mortalidad neonatal. Objetivo: Evaluar el impacto sobre la mortalidad neonatal, peso al nacer y edad gestacional, de los trastornos hipertensivos (preeclampsia e hipertensión arterial crónica), diabetes (gestacional y no gestacional) y obesidad en la gestación, en un grupo de neonatos nacidos en un hospital colombiano, entre 2005 y 2015. Métodos: Estudio de cohorte retrospectiva, con gestantes con preeclampsia (n: 326), hipertensión arterial crónica (n: 104), diabetes gestacional (n: 246) y obesidad (n: 216). Los datos fueron analizados en Stata® 11.0, empleando mediana o promedio y sus medidas de dispersión, Pruebas t, ranksum, ANOVA o Kruskal Wallis, medidas de frecuencia absolutas y relativas, Pruebas de Chi2 o exacta de Fisher. Para estimar la correlación entre las variables de exposición empleamos el Coeficiente de Correlación de Pearson y para estimar las asociaciones, empleamos riesgo relativo (RR) con su intervalo de confianza de 95%. La significancia estadística fue definida como un valor p<0,05. Resultados: Hallamos asociación significativa entre bajo peso al nacer y prematuridad con preeclampsia e hipertensión arterial crónica, y mayor peso al nacer con diabetes y obesidad. Hubo también asociación significativa entre mortalidad neonatal e hipertensión arterial crónica y diabetes. Conclusiones: Los trastornos hipertensivos y metabólicos afectan el peso y la edad gestacional al nacer, existiendo asociación significativa entre mortalidad neonatal e hipertensión arterial crónica y diabetes.

Background: Hypertensive disorders, diabetes and obesity in pregnancy, affect weight, gestational age at birth and neonatal mortality. Objective: Assess the impact on neonatal mortality, birth weight and gestational age, hypertensive disorders (pre-eclampsia and chronic hypertension), diabetes (gestational and non-gestational) and obesity in pregnancy of infants born colombian hospital between, 2005 and 2015. Methods: Retrospective cohort study with pregnant women with preeclapmsia (n: 326), chronic hypertension (n: 104), gestational diabetes (n: 246) and obesity (n: 216). The data were analyzed in Stata 11.0 using median or average and dispersion measures, t tests, ranksum, ANOVA or Kruskal Wallis, measures absolute and relative frequency, Chi2 tests or Fisher exact. To estimate the correlation between exposure variables we used the Pearson correlation coefficient and to estimate associations employ relative risk (RR) with confidence interval of 95%. Statistical significance was defined as p <0.05. Results: We found a significant association between low birth weight and prematurity with preeclampsia and chronic hypertension, and higher birth weight with diabetes and obesity. There was also significant association between neonatal mortality and chronic diabetes and hypertension. Conclusions: Hypertensive and metabolic disorders affect weight and gestational age at birth, and there is significant association between neonatal mortality and chronic diabetes and hypertension.

Epidemiología de la prematuridad, sus determinantes y prevención del parto prematuro / Epidemiology of prematurity, its determinants and prevention of preterm birth

La prematuridad es un grave de problema de salud pública por la gran morbilidad y mortalidad que generan, además, de los elevados costos económicos y sociales que ocasiona su atención. A nivel mundial, aproximadamente uno de cada diez neonatos nacen prematuros. Sus determinantes son múltiples. En el parto prematuro están involucrados además de los determinantes biológicos, los que son responsabilidad del sector salud y los que son responsabilidad del estado, como son los determinantes políticos, ambientales, sociales y económicos. Es por ello que la prevención y el tratamiento de la prematuridad debe ser una política pública obligada para todas las naciones, e involucra a muchos actores. Las estrategias empleadas para prevenir y tratar al parto prematuro son amplias y van desde los cuidados preconcepcionales, hasta la atención del parto y del neonato en el periodo postnatal.

Prematurity is a serious public health problem by the high morbidity and mortality also generated high economic and social costs caused by its staff. Globally, about one in ten infants born prematurely. Its determinants are numerous. In preterm birth are involved in addition to biological determinants, which are the responsibility of the health sector and which are the responsibility of the state, such as political, environmental, social and economic determinants. That is why prevention and treatment of prematurity should be a public policy required for all nations, and involves many actors. The strategies used to prevent and treat premature birth are spacious and range from preconception care, to care delivery and newborn in the postnatal period.

Epidemiología de la prematuridad y sus determinantes, en una población de mujeres adolescentes y adultas de Colombia / Epidemiology of prematurity and its determinants in a population of adolescent and adult women in Colombia

Antecedentes: La prematuridad es considerada actualmente una prioridad en salud pública para algunos países. Objetivo: Describir la prevalencia del parto prematuro y sus determinantes, en una población de gestantes adolescentes y adultas, que tuvieron su único o último parto en la Fundación Hospital San José de Buga, Colombia, entre los años 2010 a 2015. Métodos. Estudio de casos y controles realizado con 11.881 neonatos mujeres adolescentes y adultas. Los datos fueron analizados en Stata® 11.0, empleando para variables cuantitativas, mediana o promedio y sus medidas de dispersión, comparadas mediante pruebas t, Ranksum, ANOVA o Kruskal Wallis, de acuerdo a su distribución y para variables categóricas; medidas de frecuencia absolutas y relativas, comparadas mediante Pruebas de Chi2 o exacta de Fisher. Para estimar las asociaciones empleamos Odds Ratio con sus intervalos de confianza de 95% y para el análisis multivariado la regresión logística. La significancia estadística fue definida como un valor p<0,05. Resultados. La prevalencia de prematuridad fue 11,4%. Después del análisis multivariado, los determinantes asociados a prematuridad fueron etnia indígena-afrocolombiana o mulato, número de controles prenatales igual o inferior a 6, periodo intergenésico inferior a 2 años, embarazo múltiple, preeclampsia, oligohidramnios, restricción del crecimiento intrauterino y hemorragia del tercer trimestre (incluye desprendimiento prematuro de placenta). Conclusiones. La prematuridad es el resultado de una compleja red de determinantes individuales, sociales, culturales y gestacionales que interactúan, por lo que para su prevención se debe no sólo trabajar en medidas de salud, sino en elaboración de políticas y planes de acción integral.

Background: Prematurity is currently considered a public health priority for some countries. Objective: To describe the prevalence of preterm birth and its determinants in a population of adolescent and adult mothers who had their sole or last delivery in the Fundación Hospital San José de Buga, Colombia, between 2010-2015. Methods: Case-control study conducted with 11,881 infants adolescent and adult women. The data were analyzed in Stata 11.0, using quantitative, medium or average and dispersion measures variables compared using t tests, Ranksum, ANOVA or Kruskal Wallis, according to distribution and for categorical variables, frequency measurements absolute and relative, compared with Chi2 tests or Fisher exact. To estimate associations employ odds ratio with confidence intervals of 95% and multivariate analysis logistic regression. Statistical significance was defined as p <0.05. Results: Prematurity prevalence was 11.4%. After multivariate analysis, the determinants associated with prematurity were indigenous-Afro-Colombian or mulatto ethnicity, number of prenatal visits equal to or less than 6, less than two years intergenesic period, multiple pregnancy, preeclampsia, oligohydramnios, IUGR and bleeding of the third quarter (includes abruption). Conclusions: Prematurity is the result of a complex network of individual, social, cultural and gestational determinants that interact, so that prevention is due not only work on health measures, but in developing policies and plans integral action.

Caracterización de ALTE en neuropediatría. Hospital La Misericordia, Bogotá, Colombia, 2009-2013 / Characterization of ALTE in pediatric neurology. Hospital La Misericordia, Bogotá, Colombia, 2009-2013

Introducción: El síndrome de ALTE es una condición que amenaza la vida de los lactantes; requiere diagnóstico y manejo adecuado para evitar complicaciones o muerte, y sus causas son numerosas, entre ellas: gastrointestinales, respiratorias, neurológicas y otras; las patologías neurológicas representan la tercera causa en la mayoría de estudios. Objetivo: Describir las características de la población de pacientes que consultaron al Hospital de la Misericordia (HOMI) de Bogotá por un episodio de ALTE y que fueron valorados por la especialidad de neuropediatría en el período 2009 a 2013. Materiales y métodos: Se realizó un estudio descriptivo de corte transversal, en una población de 107 pacientes con diagnóstico de ALTE; se determinaron los datos sociodemográficos, características, causas y tratamientos de ALTE; se utilizó el programa SPSS 22. Resultados: La etiología neurológica de ALTE correspondió al 16,8%, correspondiente a crisis epilépticas, trastornos respiratorios de origen central y sangrados de sistema nervioso central. Ocupa el tercer lugar en etiologías, después de las causas gastrointestinales y respiratorias. Conclusión: Es importante definir el diagnóstico y tratamiento de los pacientes con ALTE, pues existe alto riesgo de morbimortalidad asociada. Deben evaluarse factores neurológicos, y no solo gastrointestinales o respiratorios, que ayuden a definir la etiología y evitar complicaciones.

Introduction: ALTE is a condition that threatens the lives of infants; requires diagnosis and appropriate management to avoid complications and / or death. There are numerous causes among which are gastrointestinal, respiratory, and neurological and others. Being the third cause, neurological pathologies in most studies. Objective: To describe the characteristics of the population of patients admitted to Hospital de la Misericord HOMI Bogota, for ALTE and were valued by the specialty of pediatric neurology in the period 2009-2013. Materials and methods: A descriptive cross-sectional study was conducted, with a population of 107 patients with a diagnosis of ALTE; sociodemographic data, characteristics, causes and treatments of ALTE were determined. SPSS 22 software was used. Results: The etiology of neurological ALTE corresponded to 16.8%, corresponding to seizures, respiratory disorders of central origin and CNS bleeds. Ranking as third in etiology below gastrointestinal and respiratory causes. Conclusion: It is important to define the diagnosis and treatment of patients with ALTE, as there is a high risk of morbidity and mortality associated. Factors not only neurological and gastrointestinal or respiratory, to help define the etiology and avoid complications should be evaluated.

Ataxia aguda en la población pediátrica de la Fundación Hospital de laMisericordia 2009-2013 / Acute Ataxia in the Pediatric Population of the Fundacion Hospital de la Misericordia 2009-2013

La ataxia aguda (AA) en la población pediátrica generalmente es secundaria a disfunción cerebelosade origen inmunológico. En urgencias, la rápida detección de patologías de menor frecuencia y mayorgravedad que requieren tratamiento específico es prioridad.Objetivos: Describir la etiología de la AA en los pacientes valorados por Neuropediatría en la FundaciónHospital la Misericordia entre los años 2009 y 2013.Métodos y Materiales: Estudio descriptivo tipo serie de casos. Revisión retrospectiva de historias clínicas depacientes de 1 mes a 18 años con diagnóstico definitivo de AA. Análisis de datos mediante SPSS 21, medidasde tendencia central, Kaplan Meier y prueba de Log Rank.Resultados: Se recopilaron 48 casos, de los cuales el 91,67% fue de origen cerebeloso. El diagnóstico etiológicomás frecuente fue cerebelitis o romboencefalitis viral en 25%, seguido de intoxicación aguda y post infecciosa(20,5% cada una). En cuanto a pronóstico, el 60.4 % tuvo una recuperación completa, siendo esta más rápidaen la ataxia postinfecciosa, tóxica y post traumática.Discusión: La disfunción cerebelosa fue la causa más frecuente de ataxia, los diagnósticos etiológicos principalesfueron ataxia de origen infeccioso y post infeccioso, el antecedente de infección 1 a 30 días antes del iniciode los síntomas neurológicos fue positivo en 41.67 %, lo que sugiere un importante papel de la inmunidad.Conclusiones: La mayoría de las ataxias agudas son secundarias a disfunción cerebelosa infecciosa, inmunológicao tóxica; el pronóstico depende de la etiología y generalmente es benigno...