Academic literature on the topic 'Terson, syndrome'

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Journal articles on the topic "Terson, syndrome"

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Seif, Gamal I., Joshua C. Teichman, Kesava Reddy, Charmaine Martin, and Amadeo R. Rodriguez. "Incidence, Morbidity, and Mortality of Terson Syndrome in Hamilton, Ontario." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 5 (September 2014): 572–76. http://dx.doi.org/10.1017/cjn.2014.7.

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AbstractObjectiveEvaluate the incidence, neurologic morbidity, and mortality of patients with Terson syndrome.MethodsConsecutive patients admitted to the Hamilton General Hospital from May 2012 to May 2013 with a diagnosis of spontaneous subarachnoid hemorrhage (SAH) were recruited. Funduscopic examinations were performed under pharmacological mydriasis. Outcome measures included: (1) the presence or absence of Terson syndrome; (2) The Glasgow Coma Scale (GCS), Hunt and Hess scale (H&H), and SAH Fisher score upon admission to the hospital; (3) the modified Rankin score upon discharge; and (4) and all-cause mortality.ResultsForty-six patients were included and 10 had Terson syndrome (21%). The median H&H, GCS, and Fisher scores were 4, 6.5, and 4.0 for patients with Terson syndrome vs. 2, 14, and 3 for patients without Terson syndrome (p=0.0032, 0.0052, and 0.031), respectively. The median Rankin score was 6 for patients with Terson syndrome vs. 3.5 for patients without Terson syndrome (p=0.0019). The odds of all-cause mortality with Terson syndrome vs. no Terson syndrome was 12: 1 (95% confidence interval 2.33-61.7), p =0.003. Only four of the 10 patients with Terson syndrome survived.ConclusionsBased on this study, approximately one-fifth of patients admitted to the hospital with a spontaneous SAH could have Terson syndrome. Patients with Terson syndrome have significantly worse GCS and H&H scores upon admission to the hospital, lower modified Rankin scores upon discharge, and greater mortality. Thus, Terson syndrome is not rare among patients with SAH and carries a worse prognosis.
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Ogawa, Tsukihiko, Takashi Kitaoka, Yoshinori Dake, and Tsugio Amemiya. "Terson syndrome." Ophthalmology 108, no. 9 (September 2001): 1654–56. http://dx.doi.org/10.1016/s0161-6420(01)00673-x.

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Mills, Monte D. "Terson syndrome." Ophthalmology 105, no. 12 (December 1998): 2161–62. http://dx.doi.org/10.1016/s0161-6420(98)91200-3.

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Kuhn, Ferenc, Robert Morris, C. Douglas Witherspoon, and Viktória Mester. "Terson syndrome." Ophthalmology 105, no. 3 (March 1998): 472–77. http://dx.doi.org/10.1016/s0161-6420(98)93030-5.

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Middleton, Kim, Peter Esselman, and P. Chuwn Lim. "Terson Syndrome." American Journal of Physical Medicine & Rehabilitation 91, no. 3 (March 2012): 271–74. http://dx.doi.org/10.1097/phm.0b013e3182328792.

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Troumani, Y., L. Beral, F. Glatre, E. Finke, and T. David. "Syndrome de Terson." Journal Français d'Ophtalmologie 37, no. 6 (June 2014): 501. http://dx.doi.org/10.1016/j.jfo.2013.12.011.

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Elmi Sadr, Navid, Bijan Samavat, Payam Mehrian, and Alireza Hedayatfar. "Intraocular Silicone Oil Masquerading as Terson Syndrome." Case Reports in Ophthalmological Medicine 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/4942109.

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Introduction. Terson syndrome is described as intraocular hemorrhage in association with any type of intracranial hemorrhage and is associated with higher mortality rate and vision loss. Intraocular hemorrhage in Terson syndrome may be diagnosed using computed tomography but there are false positive results. Silicone oil which is widely used for internal tamponade of complicated retinal detachments has high attenuation on computed tomography and hyperintensity on T1-weighted magnetic resonance imaging that can mimic intraocular hemorrhage. This report shows that silicone oil is another origin of false positive results in interpreting CT findings for detecting Terson syndrome.Case Report. A 71-year-old diabetic woman presented with loss of consciousness. Brain computed tomography revealed right cerebellar hemorrhage and ventricular hemorrhage and hyperdensity in vitreous cavity of the left eye that was initially interpreted as vitreous hemorrhage. Terson syndrome was the initial diagnosis but ophthalmoscopic examination and brain MRI showed that the left eye had silicone oil tamponade.Conclusion. Without knowing the history of previous vitreoretinal surgery, CT scan findings of intraocular silicone oil may be interpreted as vitreous hemorrhage. In patients with concomitant intracranial hemorrhage, it can masquerade as Terson syndrome.
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Hoving, Eelco W., Mehrnoush Rahmani, Leonie I. Los, and Victor W. Renardel de Lavalette. "Bilateral retinal hemorrhage after endoscopic third ventriculostomy: iatrogenic Terson syndrome." Journal of Neurosurgery 110, no. 5 (May 2009): 858–60. http://dx.doi.org/10.3171/2008.6.17610.

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A serious ophthalmological complication of an endoscopic third ventriculostomy that created an iatrogenic Terson syndrome is described. A patient with an obstructive hydrocephalus was treated endoscopically, but due to the inadvertent use of a pressure bag during rinsing, in combination with a blocked outflow channel, a steep rise in intracranial pressure occurred. Postoperatively the patient experienced disturbed vision caused by bilateral retinal hemorrhages, and an iatrogenic Terson syndrome was diagnosed. The pathogenesis of Terson syndrome is discussed based on this illustrative case.
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Karadzic, Jelena, Igor Kovacevic, Ivan Stefanovic, and Dijana Risimic. "Terson’s syndrome: A report of two cases." Srpski arhiv za celokupno lekarstvo 143, no. 9-10 (2015): 595–98. http://dx.doi.org/10.2298/sarh1510595k.

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Introduction. Vitreous or retinal hemorrhage occurring in association with subarachnoid hemorrhage is known as Terson?s syndrome. In Terson?s syndrome, intracranial hemorrhages are followed by intraocular hemorrhage, classically in the subhyaloid space, but may also include subretinal, retinal, preretinal, and vitreal collections. Vitreous hemorrhage recovery is usually spontaneous in six to 12 months, otherwise vitrectomy is considered. Outline of Cases. We report of two cases of Terson?s syndrome. The first was in a hypertensive middleaged female, following anterior communicating artery aneurismal subarachnoid hemorrhage, after postneurosurgical interventions. The second case report was of a young male who suffered from the bilateral vitreous hemorrhage after a severe traumatic brain injury. Conclusion. Terson?s syndrome should be considered in patients who had previous cerebral hemorrhage and are referred to eye specialist because of loss of vision. However, this phenomenon has only rarely been described in association with subdural and epidural hematomas or traumatic subarachnoid hemorrhage.
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El Kettani, M., A. Moussair, L. El Maaloum, D. Lahbil, H. Lamari, A. El Kettani, L. Rais, A. Amraoui, and K. Zaghloul. "736 Syndrome de Terson." Journal Français d'Ophtalmologie 31 (April 2008): 220. http://dx.doi.org/10.1016/s0181-5512(08)71335-4.

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Dissertations / Theses on the topic "Terson, syndrome"

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FARGEIX, CATHERINE. "Syndrome de terson post-traumatique et vitrectomie." Saint-Etienne, 1989. http://www.theses.fr/1989STET6402.

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Belso, Laurence. "Syndrome de Terson : étude rétrospective à propos de quatre cas." Montpellier 1, 1997. http://www.theses.fr/1997MON11163.

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JOUY, VALERIE. "A propos d'un cas de syndrome de terson par anevrysme de l'origine du tronc basilaire." Toulouse 3, 1990. http://www.theses.fr/1990TOU31020.

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Terry, B. R., Gayatri Jaishankar, Jennifer Gibson, and Debra Q. Mills. "Retinal Hemorrhage: More Than Meets the Eye." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/8864.

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Vetterle, Martin Tobias [Verfasser], and Wolfgang [Akademischer Betreuer] Schrader. "Ergebnisse der Pars-plana-Vitrektomie bei Terson-Syndrom unter ophthalmologischen und neurologischen Gesichtspunkten / Martin Vetterle. Betreuer: Wolfgang Schrader." Würzburg : Universitätsbibliothek der Universität Würzburg, 2011. http://d-nb.info/1018163417/34.

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Heidemann, Luciana Alonzo. "Prevalência de síndrome metabólica aos dois anos de idade corrigida em pré-termos de muito baixo peso ao nascer." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2011. http://hdl.handle.net/10183/55161.

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Introdução: A Síndrome Metabólica (SM) é um grupo de distúrbios que inclui obesidade, resistência insulínica, dislipidemia e hipertensão. Está associada com o desenvolvimento subsequente de doença cardiovascular e diabete tipo 2. Estudos mostram relação entre baixo peso ao nascer e SM na vida adulta, mas não há estudos sobre a prevalência da SM em pré-termos já na infância precoce. Objetivo: Medir a prevalência da SM aos dois anos de idade corrigida de pré-termos com peso de nascimento inferior ou igual a 1.500 gramas e os fatores associados. Metodologia: Estudo transversal aninhado em uma coorte já existente que incluiu crianças em acompanhamento regular no ambulatório de seguimento de prematuros de hospital terciário aos dois anos de idade corrigida. O diagnóstico de SM foi feito com a presença de três ou mais dos critérios de Cook e colaboradores: circunferência abdominal ≥ percentil 90, glicemia de jejum ≥ 100mg/dl, triglicerídeos ≥ 110mg/dl, HDL colesterol ≤ 40mg/dl e pressão arterial ≥ percentil 90. Estudo aprovado pelo CEP da instituição: 09226. Testes empregados: Qui-quadrado, t de Student, Mann-Whitney e Regressão Logística. Resultados: 235 pré-termos de muito baixo peso foram elegíveis ao programa de seguimento. Destes, 9,4% falharam ao seguimento. A prevalência de SM foi de 15,1%. Doença hipertensiva materna, diabetes gestacional, sexo, idade gestacional, ser pequeno para idade gestacional, sepse precoce e tardia, displasia broncopulmonar, nutrição parenteral com aminoácidos nas primeiras 24 horas de vida, enterocolite necrosante, hemorragia e leucomalácia periventricular, persistência do canal arterial, alimentação no primeiro ano de vida, catch-up de peso, renda e escolaridade materna foram semelhantes entre os grupos. Crianças filhas de mães que tiveram infecção urinária ou ovular e a presença de sobrepeso ou obesidade aos dois anos de idade corrigida apresentaram uma maior prevalência de SM em análises univariadas. Usando a Regressão Logística, apenas sobrepeso ou obesidade aos dois anos de idade corrigida tiveram associação independente com a presença precoce de SM em pré-termos de muito baixo peso. Conclusão: A SM já se encontra presente em pré-termos de muito baixo peso aos dois anos de idade e é muito mais frequente do que o esperado. Na análise univariada, encontramos uma associação positiva da SM com fatores intrauterinos como infecção materna. Provavelmente esta situação aumenta o cortisol fetal, programando a SM. Além do mais, a presença de sobrepeso e/ou obesidade é um fator independente para maior prevalência da SM.
Background: Metabolic syndrome (MS) is a group of disorders which includes obesity, insulin resistance, dyslipidemia and hypertension. It is associated with subsequent development of cardiovascular disease and type 2 diabetes. Some studies suggest a relationship between low birth weight and onset of MS in adulthood, however there is no study showing MS prevalence in preterm, even in early childhood. Aim: To assess the prevalence of MS in very low birth weight preterm infants at two years corrected age and identify factors possibly associated with a higher occurrence of MS. Methods: A prospective cohort study of very low birth weight infants at two years corrected age who attended to a preterm follow up clinic of a tertiary hospital. To define Metabolic syndrome we considered the criteria of Cook et al.: Waist circumference ≥ 90th percentile, fasting glucose ≥ 100mg/dl, triglycerides ≥ 110mg/dL, HDL cholesterol ≤ 40 mg/dl and blood pressure ≥ 90th percentile. The presence of three or more of these criteria defines the MS diagnosis. This study was approved by ethics committee of the institution (09226). Chi-square, Student t, Mann-Whitney tests and Logistic Regression were used. Results: 235 very low birth weight preterm infants were eligible to follow up program. Of these, 9.4% failed. MS prevalence was 15.1%. Maternal hypertensive disorders, gestational diabetes, gender, gestational age, small for gestational age, early and late sepsis, bronchopulmonary dysplasia, parenteral nutrition with amino acids in the first 24 hours of life, necrotizing enterocolitis, hemorrhage and periventricular leukomalacia, patent ductus arteriosus, feeding at discharge and during the first year of life, income and maternal education were similar between groups. Children of mothers who had urinary tract infection or chorioamnionitis and presence of overweight / obesity at 2 years CA showed a higher MS prevalence in univariate analyses. Using Logistic Regression, only overweight / obesity at 2 years CA was independently associated with the early presence of MS in very low birth weight infants. Conclusion: MS is already present in preterm of very low birth weight at 2 years corrected age and is higher than expected. In the univariate analysis MS was associated with intrauterine factors such as maternal infection. This situation would lead to an increase in fetal cortisol, programming MS. Furthermore, the early-onset overweight and obesity is an independent risk factor to MS in those newborns.
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Lyra, Priscila Pinheiro Ribeiro. "Análise de polimorfismos do gene que codifica a proteína B do surfactante: comparação entre recém-nascidos de termo sadios e recém-nascidos pré-termo com síndrome do desconforto respiratório." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-13102014-105443/.

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A etiologia da síndrome do desconforto respiratório (SDR) é considerada multifatorial e multigênica. A proteína B do surfactante (SP-B) é essencial para a função pulmonar normal. O gene responsável pela produção da SP-B está localizado no braço curto do cromossomo 2 (2p12->p11.2), estendendo-se por aproximadamente por 9.5 Kilobases e contém 11 exons. A presença de polimorfismos e mutações em genes dos componentes do surfactante, particularmente no gene da SP-B, parece estar associada à SDR. Objetivos: Determinar a freqüência de polimorfismos do gene que codifica a proteína B do surfactante no DNA de recém nascidos pré-termo portadores de SDR e de recémnascidos de termo sadios, comparar as freqüências desses polimorfismos entre os dois grupos e avaliar se existe alguma relação entre sexo, raça e SDR. Casuística e Métodos: Foram incluídos no estudo 150 RN, sendo 50 pré-termo portadores de SDR com idades gestacionais variando entre 28 e 33 semanas e 6 dias, e 100 RN de termo clinicamente sadios com idades gestacionais variando de 37 a 41 semanas e seis dias, no período de junho de 2001 a julho de 2004. Foram analisados quatro polimorfismos: A/C no nucleotídeo - 18; C/T no nucleotídeo 1580; A/G no nucleotídeo 9306 e G/C no nucleotídeo 8714. Os polimorfismos foram determinados através da amplificação dos segmentos de DNA genômico por reação em cadeia da polimerase e posterior genotipagem. Os genótipos foram definidos através da análise dos produtos obtidos a partir de reações com enzimas de S . 22 restrição [PCR-based converted restriction fragment length polymorphism (cRFLP)]. Resultados: O grupo controle foi constituído por 100 RN de termo aparentemente saudáveis; 42(42%) do sexo feminino e 58(58%) do sexo masculino; 39(39%) da raça branca e 61(61%) da raça não branca. O peso variou de 2280g a 4.740g (média de 3.239,9g), e a idade gestacional variou de 37 a 41 semanas e seis dias (média de 39 semanas e 3 dias). O grupo SDR foi composto por 50 RNPT, sendo 21(42%) do sexo feminino e 29(58%) do sexo masculino; 28(56%) eram da raça branca e 22(44%), não brancos. O peso variou de 640g a 2.080g (média de 1273g); a idade gestacional média foi de 31 semanas e dois dias, tendo variado de 28 semanas a 33 semanas e seis dias. Foi encontrada uma diferença estatisticamente significante quando comparados os dois grupos e a variável raça isoladamente no polimorfismo G/C 8714 (p=0,028). Quando a variável sexo foi analisada isoladamente, não houve diferença estatisticamente significante dos polimorfismos entre os dois grupos. As freqüências dos genótipos dos outros três polimorfismos estudados foram muito similares nos dois grupos, não tendo sido encontrada diferença estatisticamente significante quando as variáveis sexo e raça foram avaliadas conjuntamente. Conclusão: A análise do polimorfismo G/C 8714 mostrou que em indivíduos da raça branca, o genótipo GG foi apenas encontrado no grupo SDR, sugerindo que a sua presença possa se constituir em um possível fator de risco para a doença, enquanto que o genótipo GC foi mais prevalente no grupo controle indicando a possibilidade desse genótipo ser um fator protetor
The etiology of respiratory distress syndrome (RDS) is multifactorial and multigenic. Surfactant protein B (SP-B) is essential for normal lung function. The human SP-B gene is located on the short arm of chromosome 2 (2p12->p11.2), encompasses approximately 9.5 kilobases and have 11 exons. Polymorphisms and mutations in the genes that encode the surfactant components, particularly the SP-B gene, have been associated to the pathogenesis of RDS. Aims: To analyze SP-B gene polimorfisms frequencies in preterm babies with RDS and healthy term newborns, to compare the polymorphisms frequencies between both groups and to evaluate if there are differences related to sex, race and RDS. Material and Methods: We included 150 neonates, 50 preterm with RDS and gestational ages ranging from 28 weeks to 33 weeks and 6 days, and 100 healthy term newborns with gestational ages ranging from 37 weeks to 41 weeks and 6 days, during June 2001 to July 2004. Four SP-B gene polymorphisms were analyzed: A/C at - 18, C/T at 1580; A/G at 9306 and G/C at nucleotide 8714. The polymorphisms were detected by PCR amplification of genomic DNA and genotyping. The genotypes were determined using PCR-based converted restriction fragment length polymorphism (cRFLP). Results: The control group comprised 100 apparently healthy term newborns; 42(42%) were female and 58(58%) male; 39(39%) were Whites and 61(61%) non-Whites. Weight ranged from 2280g to 4.740g (mean 3.239,9g); gestational age ranged from 37 weeks to 41 weeks and six days (mean 39 weeks and 3 days). The RDS group comprised 50 preterm neonates, 21(42%) female and 29(58%) male; 28(56%) were Whites and 22(44%) non-Whites. Weight ranged from 640g to 2.080g (mean 1273g); mean gestational age was 31 weeks and two days (range, 28-33 weeks and six days). All genotypes frequencies were similar among both groups when sex and race were analyzed together. When race was analyzed separately, there was a statistically significant difference between both groups in the polymorphism G/C at 8714 (p=0,028). There was no difference between both groups in all polymorphisms when sex was analyzed separately. Conclusions: The analysis of the SP-B polymophism G/C 8714 showed that in white neonates the genotype GG was only found in the RDS group and the genotype GC was more frequently found in controls. This suggests that genotype GG could be a risk factor while GC might be a protective genotype for the development of the disease
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Lyra, Priscila Pinheiro Ribeiro. "Análise de polimorfismos do gene que codifica a proteína B do surfactante: comparação entre recém-nascidos pré-termo com e sem síndrome do desconforto respiratório." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-24082010-171621/.

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A síndrome do desconforto respiratório (SDR) é causada pela deficiência transitória de surfactante pulmonar em recém-nascidos (RN) prematuros nos primeiros dias de vida. Estudos sugerem que a etiologia da SDR seja multifatorial e multigênica. A proteína B do surfactante (SP-B) é fundamental para o metabolismo do surfactante e para uma função pulmonar normal. A presença de polimorfismos e mutações em genes dos componentes do surfactante, particularmente no gene da SP-B, parece estar associada à SDR. Objetivos: Determinar a freqüência de polimorfismos do gene que codifica a proteína B do surfactante no DNA de recém nascidos pré-termo com e sem SDR, comparar as freqüências desses polimorfismos entre os dois grupos e avaliar se existe alguma relação entre sexo, raça e SDR. Casuística e Métodos: Foram incluídos no estudo 151 RNPT, sendo 79 sem SDR com idades gestacionais variando entre 29 semanas e 35 semanas e 6 dias e 72 RN pré-termo com SDR com idades gestacionais variando de 26 a 35 semanas. Foram analisados quatro polimorfismos: A/C no nucleotídeo - 18; C/T no nucleotídeo 1580; A/G no nucleotídeo 9306 e G/C no nucleotídeo 8714. Os polimorfismos foram determinados através da amplificação dos segmentos de DNA genômico por reação em cadeia da polimerase e posterior genotipagem. Os genótipos foram definidos através da análise dos produtos obtidos a partir de reações com enzimas de restrição [PCR-based converted restriction fragment length polymorphism (cRFLP)]. Resultados: O grupo Controle foi constituído por 79 RN pré-termo sem SDR; sendo 42 (53,2%) do sexo feminino e 37 (46,8%) do sexo masculino; 34 (43%) da raça negra, 16(20,3%) da raça branca e 29(36,7) de indivíduos pardos. O peso variou de 1170g a 3260 , e a idade gestacional variou de 29 semanas a 35 semanas e seis dias (média de 33 semanas e 6 dias).O grupo SDR foi composto por 72 RNPT, sendo que 31 (43%) do sexo feminino e 41 (57%) do sexo masculino; 31(43%) da raça negra, 16 (14%) da raça branca e 31(43%) de indivíduos pardos. O peso variou de 614g a 2.410g ; a idade gestacional média foi de 32 semanas , tendo variado de 26 semanas a 35 semanas. O modelo de regressão logística múltipla, utilizado para avaliar a contribuição das diversas variáveis na probabilidade de ocorrer SDR, demonstrou que a idade gestacional foi a variável que mais contribuiu para a ocorrência da patologia, e que o genótipo AG do polimorfismo A/G na posição 9306 foi um fator protetor para a doença nesta população (OR 0.1681; IC 95% 0.0426 - 0.6629). Não foram observadas diferenças entre as freqüências dos demais polimorfismos avaliados entre os 2 grupos de recém-nascidos, bem como diferenças quanto à raça e sexo. Conclusões: A presença do genótipo AG do polimorfismo A/G na posição 9306 do gene que codifica a proteína B do surfactante foi fator protetor para o desenvolvimento da síndrome do desconforto respiratório em recém-nascidos da cidade de Salvador-Bahia. Os polimorfismos A/C no nucleotídeo - 18, C/T no nucleotídeo 1580, e G/C no nucleotídeo 8714 presentes no referido gene não estiveram associados à síndrome do desconforto respiratório em recém-nascidos na amostra estudada.
The respiratory distress syndrome (RDS) is caused by surfactant transient deficiency in preterm babies soon after birht. Studies sugest that RDS etiology is multifactorial and multigenic. Surfactant protein B (SP-B) is essential for surfactant metabolism and fornormal lung function. Polymorphisms and mutations in the genes that encode the surfactant components, particularly the SP-B gene, have been associated to the pathogenesis of RDS. Aims: To analyze SP-B gene polimorfisms frequencies in preterm babies with RDS and healthy term newborns, to compare the polymorphisms frequencies between both groups and to evaluate if there are differences related to sex, race and RDS. Material and Methods: We included 151 neonates, 79 preterm babies without RDS and gestational ages ranging from 26 weeks to 35 weeks , and 72 preterm newborns with RDS, gestational ages ranging from 29 weeks to 35 weeks and 6 days. Four SP-B gene polymorphisms were analyzed: A/C at - 18, C/T at 1580; A/G at 9306 and G/C at nucleotide 8714. The polymorphisms were detected by PCR amplification of genomic DNA and genotyping. The genotypes were determined using PCR-based converted restriction fragment length polymorphism (cRFLP). Results: The control group comprised 79 preterm babies without RDS; 42(53,2%) were female and 37(46,8%) male; 34(43%) were black, 16(20,3) were Whites and 29(36.7%) non- Whites/non black. Weight ranged from 1.170g to 3.260g ; gestational age ranged from 29 weeks to 35 weeks and six days (mean 33 weeks and 6 days). The RDS group comprised 72 preterm neonates, 31(43%) female and 41(57%) male; 31(43%) were black, 16(14%) were Whites and 31(43%) non-Whites/non black. Weight ranged from 614g to 2.410g ; mean gestational age was 32 weeks (range, 26-35 weeks). The logistic regression model showed that gestational age was the variable that most contributed to the ocurrence of the respiratory distress syndrome and the AG genotype of the polymorphism A/G at 9306 was a protector factor for the disease in the studied population (OR 0.1681; CI 95% 0.0426 - 0.6629). We did not detect differences between the frequencies of the other evaluated polymorphisms between both groups of newborns. Conclusions: The presence of AG genotype at 9306 of the surfactant protein B (SP-B) gene was a protector factor for the development of the respiratory distress syndrome in newborns from the city of Salvador-Bahia. The polymorphisms A/C at nucleotide - 18, C/T at 1580, and G/C at nucleotide 8714 from the SP-B gene were not associated with respiratory distress syndrome in the studied population.
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Komatsu, Daniela Franco Rizzo. "Estudo controlado e randomizado entre o uso de ventilação por pressão positiva intermitente e pressão positiva contínua em vias aéreas em recém-nascidos pré-termo após a extubação traqueal." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-06112007-100225/.

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Objetivos: Analisar a frequência de falha da extubação em recém-nascidos pré-termo em ventilação mecânica convencional após a extubação traqueal nos grupos submetidos a ventilação por pressão positiva intermitente por via nasal (nIPPV) e pressão positiva contínua em vias aéreas (nCPAP). Métodos: Foram estudados 72 recém-nascidos pré-termo portadores de insuficiência respiratória, com idade gestacional 750 gramas, que necessitaram de entubação traqueal e ventilação mecânica. Após terem preenchido os critérios de extubação, os recém-nascidos foram submetidos a nIPPV (n=36) ou nCPAP (n=36) de acordo com o resultado da randomização. Os parâmetros iniciais para os RN randomizados para nIPPV foram: FR = 12 ipm; PIP = 16 cm H20; PEEP= 6 cm H20; FiO2 ? 40%, e para aqueles randomizados para nCPAP foram P=6 cm H2O; FiO2 < 40%. O estudo foi finalizado após um tempo de extubação de 72 horas ou quando o RN preenchesse os critérios de falha na extubação. O projeto de pesquisa foi aprovado pela Comissão de Ética de ambos os Serviços. Resultados: A grande maioria dos RN recebeu pelo menos uma dose de surfactante exógeno (80,5% no grupo nIPPV e 83,3% no grupo nCPAP, P= 1). O tempo médio de permanência em ventilação mecânica também foi semelhante (6,2 e 7,3 dias, P= 0,59, respectivamente). Entre os 36 RN randomizados para nIPPV, 6 (16,6%) apresentaram falha de extubação em comparação a 11 (30,5%) dos 36 RN randomizados para nCPAP. Apesar de se ter observado redução relativa de risco de falha de extubação da ordem de 45% (IC 95%: 0,23 a 1,32) a favor da nIPPV, esta diferença não alcançou significância estatística. Constatamos uma chance de falha de extubação de 4,38 vezes no grupo nCPAP quando comparado ao grupo nIPPV após excluírmos os RN com peso de nascimento inferior a 1000 gramas, sendo esta diferença estatisticamente significativa (P= 0,045).Complicações gastrointestinais e neurológicas, além de outras complicações, não ocorreram nos recém nascidos pré-termo submetidos à nIPPV ou nCPAP após a extubação. Conclusões: Embora a distribuição de frequências de falha da extubação tenha mostrado numericamente um menor índice de falha nos RNPT submetidos a nIPPV em relação àqueles submetidos a nCPAP, não houve diferença estatísticamente significante entre os dois modos de suporte ventilatório após a extubação. Ao excluirmos da análise os RN com peso de nascimento inferior a 1000 gramas constatamos um aumento estatisticamente significante na chance de falha no grupo nCPAP.
Objetive: To analyze the frequency of failed extubation in premature infants following mechanical ventilation placed on either nasal intermittent positive pressure ventilation (nIPPV) or nasal continuous positive airway pressure (nCPAP) after endotracheal tube removal. Methods: Seventy two premature infants with respiratory insufficiency and gestacional age 750 grams, who needed endotracheal intubation and mechanical ventilation were studied. Once the babies reached the criteria for exubation, they were randomized to either nIPPV (n=36) or to nCPAP (n=36) in accordance with the randomization resulted. The inicial settings for those randomized to nIPPV were: rate=12; PIP=16 cm H20; PEEP=6 cm H20; FiO2 < 40%, and for those randomized to nCPAP were P=6 cm H2O; FiO2 < 40%. The study ended after 72 hours or when the infants reached the criteria of failure of the extubation. Ethical Approval was obtained from the Hospital. Results: Most received at least one dose of exogenous surfactant (80,5% in the nIPPV group and 83,3% in the nCPAP group, P= 1). The average time of mechanical ventilation also was similar (6.2 and 7.3 days respectively, P= 0.59). Of the 36 infants randomized to nIPPV, six (16,6%) failed extubation in comparison to 11 (30,5%) of the 36 newborn randomized to nCPAP. Although to have itself observed relative reduction of risk failure of extubation the order of 45% (95%CI: 0,23 to 1,32) in the group nIPPV, this difference did not reach significance statistics. We verified a increaset of failure extubation of 4,38 times in the nCPAP group when compared to the group nIPPV after excluded premature infant from birthweight less than 1000 grams, this difference was significant (P = 0,045). Gastrointestinal and neurological complications, beyond other complications, had no occurred in premature infants submitted to nIPPV or nCPAP after the extubation. Conclusions: Although the distribution of frequencies has numerically shown a lesser index of failure in premature infants submitted to nIPPV in relation to those submitted to nCPAP after extubation they did not have statistical significance difference between the two ways of ventilatory support. To the excluded of the analysis premature infant with birthweight less than 1000 grams, verified an increase significant in the failure extubation in the nCPAP.group .
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Vetterle, Martin. "Ergebnisse der Pars-plana-Vitrektomie bei Terson-Syndrom unter ophthalmologischen und neurologischen Gesichtspunkten." Doctoral thesis, 2011. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-65933.

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Als Terson-Syndrom wird eine Glaskörperblutung in Kombination mit einer intrakraniellen Blutung beschrieben. Eine persistierende Glaskörperblutung ist eine Indikation zur Pars-plana-Vitrektomie(PpV). Sie ist heute mittlerweile eine etablierte Operationstechnik zur Entfernung der Glaskörperblutung, um eine rasche Visusverbesserung zu erlangen und eine schnelle Rehabilitation der neurologischen Befunde zu erreichen. In dieser Studie wurde untersucht, in wie fern eine frühzeitige Operation nach dem akuten Ereignis auf den neurologischen und ophthalmologischen Befund auswirkt. Es wurden die Krankenakten von 32 Patienten mit Terson- Syndrom ausgewertet, welche sich in einem Zeitraum von 1996-2004 einer PPV aufgrund einer Glaskörperblutung nach intrakranieller Blutung unterzogen. Es trat bei allen Augen eine Verbesserung des Visus auf. Der Visus stieg von LogMAR 1,9 (Fingerzählen) auf postoperativ LogMAR 0,551 (etwa Visus 0,3) 6 Monate nach Operation, Log MAR 0,148 1 Jahr und LogMAR 0,17 (jeweils 0,7) 3 Jahre nach der Operation an. Nach der Operation trat eine rasche Erholung des neurologischen Defizits auf. Präoperativ waren 63% auf einen Rollstuhl angewiesen. Dieser Anteil sank nach 6 Monaten auf 39% und nach drei Jahren waren es nur noch 30%. In dieser Studie konnte ein Nutzen der PpV bei Terson-Syndrom Patienten herausgearbeitet werden. Der Eingriff erwies sich als komplikationsarm. Des Weiteren kann man eine baldigere Rehabilitation des Patienten ermöglichen
The Terson´s syndrome is described as an intra-vitreous bleeding in combination with subarachnoid hemorrhage. A pars plana vitrectomy (PPV) is performed, when the vitreous hemorrhage persists. Today this technique is established for patients with Terson´s syndrome to restore the visual function and ease the further neurological rehabilitation. The findings of our retrospectively study analyzed the long term anatomical and functional results and the further neurological development. 32 patients underwent vitreous surgery (PPV) for Terson´s syndrome between 1996- 2004. Visual improvement occurred in all eyes. Visual acuity rose from LogMAR 1.9 (finger counting) to LogMAR 0.551 (VA 0.3) 6 months after surgery to LogMAR at 1 year and Log MAR 0.179(each is about 0.7) 3 years following surgery. PPV enabled rapid further neurological rehabilitation. Preoperatively 63% could neither walk with or without assistance and had to rely on a wheel chair. After 6 weeks only 39% needed a wheel chair, after 3 years only 30%. PPV for Terson´s syndrome can be successfully performed as an outpatient procedure with a low complication rate. Vitrectomy accelerates the neurological rehabilitation process
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Books on the topic "Terson, syndrome"

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Ferri, Caterina, Maria Turchese Caletti, and Federica Provini. NREM and other parasomnias. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0039.

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Parasomnias are a heterogeneous group of undesirable, but not always pathological, manifestations that accompany sleep. They consist in abnormal behaviors due to the inappropriate activation of cognitive processes or physiological systems such as the motor and/or autonomic nervous systems. In some cases, they can result in sleep disruption and injuries, with adverse health or psychosocial consequences for patients, bed-partners or both. According to the International Classification of Sleep Disorders, parasomnias are distinguished on the basis of the stage of sleep in which they appear: (1) parasomnias arising from NREM (non-rapid eye movement) sleep, which include arousal disorders (confusional arousal, sleep terror, sleepwalking) and sleep-related eating disorders; (2) parasomnias associated with REM (rapid eye movement) sleep; and (3) “other parasomnias” occurring in any sleep stage (eg, sleep enuresis, exploding head syndrome). This chapter describes the NREM parasomnias and the “other parasomnias,” underlining the more recent and significant advances that have provided a better understanding of their clinical features and pathophysiology.
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Book chapters on the topic "Terson, syndrome"

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Falco, Jeff, Sumayya J. Almarzouqi, and Andrew G. Lee, MD. "Terson Syndrome Caused by Subarachnoid Hemorrhage." In Encyclopedia of Ophthalmology, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_1296-1.

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Falco, Jeff, Sumayya J. Almarzouqi, and Andrew G. Lee. "Terson Syndrome Caused by Subarachnoid Hemorrhage." In Encyclopedia of Ophthalmology, 1786–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1296.

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Morris, R., F. Kuhn, C. D. Witherspoon, V. Mester, and J. Dooner. "Hemorrhagic Macular Cysts in Terson�s Syndrome and Its Implications for Macular Surgery." In Developments in Ophthalmology, 44–54. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000060726.

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Ossoinig, K. C., D. S. Reshef, T. A. Weingeist, J. C. Folk, and A. J. Packer. "Echographic findings in Terson’s syndrome." In Documenta Ophthalmologica Proceedings Series, 247–56. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3315-6_42.

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Lueger-Schuster, Brigitte. "Posttraumatisches Syndrom als Folge von Terrorerfahrungen am Beispiel totalitärer Staaten." In Terror und Geschichte, 223–32. Wien: Böhlau Verlag, 2011. http://dx.doi.org/10.7767/boehlau.9783205791782.223.

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Lizzi, P., S. Da Pozzo, Lucio Borzaghini, and P. Perissutti. "A-B scan echographic imaging in a case of Terson’s syndrome." In Documenta Ophthalmologica Proceedings Series, 263–68. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5802-2_29.

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"Terson Syndrome." In Ophthalmology: Current and Future Developments, edited by Adai Pérez Montesinos, 20–23. BENTHAM SCIENCE PUBLISHERS, 2017. http://dx.doi.org/10.2174/9781681084138117020007.

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"81 Terson Syndrome." In The Retina Illustrated, edited by Justis P. Ehlers and Thuy K. Le. Stuttgart: Georg Thieme Verlag, 2020. http://dx.doi.org/10.1055/b-0040-174266.

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Hawkes, Christopher H., Kapil D. Sethi, and Thomas R. Swift. "Epilepsy and Sleep Disorders." In Instant Neurological Diagnosis, 141–60. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199361953.003.0006.

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This chapter lists diagnostic clues that allow identification of various syndromes by inspection alone, such as tuberous sclerosis, Sturge Weber syndrome, lipoid proteinosis, Angelman’s syndrome, and Rett syndrome. Guides to localization and lateralization are provided, as well as the main causes of refractory seizures. Characteristic EEG patterns found in epilepsy and sleep disorders are illustrated. Diagnostic clues associated with non-epileptic attack disorders are described. Handles are exemplified for the major sleep-related disorders, such as sleep–wake transition disorder, frontal lobe seizures, night terror, catathrenia, Klein-Levine syndrome, fatal familial insomnia, and sleep paralysis.
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"Terson’s Syndrome." In Encyclopedia of Ophthalmology, 1787. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_101748.

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