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Contrast-induced encephalopathy is a neurological complication related to contrast used in endovascular procedures or computed tomography (CT). The main risk factors are arterial hypertension, diabetes mellitus, chronic kidney disease (CKD), hyperosmolar contrasts, the amount of infused contrast and its direct infusion in the posterior cerebral territory, or pathologies with blood-brain barrier damage. Symptomatology is non-specific and may present as altered level of consciousness, neurological focality or seizures. Diagnosis is done by exclusion after ischemic or hemorrhagic stroke has been ruled out; CT or MRI are useful for differentiation. Generally, it appears shortly after exposure and the symptoms lasts 48−72h with complete recovery, although cases with persistence of symptoms or longer duration have been described. Treatment consists of monitoring, supportive measures and kidney replacement therapy (KRT) with hemodialysis (HD) in patients in chronic KRT program. It is important for the nephrologist to be aware of this entity given the susceptibility of the patient on HD as well as its potential therapeutic role in these patients. Resumen: La encefalopatía por contraste es una complicación neurológica relacionada con el contraste utilizado en procedimientos endovasculares o tomografía computarizada (TC). Los principales factores de riesgo son la hipertensión arterial, la diabetes mellitus, la enfermedad renal crónica (ERC), contrastes hiperosmolares, cantidad de contraste infundida y su infusión directa en el territorio cerebral posterior, o patologías que cursen con daño de barrera hematoencefálica. La sintomatología es inespecífica y puede presentarse como alteración del nivel de conciencia, focalidad neurológica o crisis comiciales. El diagnóstico es de exclusión tras haber descartado los accidentes cerebro-vasculares isquémicos o hemorrágicos, el TC o la resonancia magnética son de utilidad para su diferenciación. Generalmente, aparece poco tiempo tras la exposición y la sintomatología dura 48−72h con recuperación completa, aunque se han descrito casos con persistencia de los síntomas o mayor duración. El tratamiento es la monitorización con medidas de soporte y la terapia de sustitución renal con hemodiálisis (HD) en aquellos pacientes en programa crónico. Es importante que el nefrólogo conozca esta entidad dada la susceptibilidad del paciente en HD así como su potencial papel terapéutico en estos pacientes.

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Fatigue is a complex, multidimensional syndrome that is prevalent in patients with acquired brain damage and has a negative impact on the neurorehabilitation process. It presents from early stages after the injury, and may persist over time, regardless of whether sequelae have resolved. Fatigue is conditioned by upper neuronal circuits, and is defined as an abnormal perception of overexertion. Its prevalence ranges from 29% to 77% after stroke, from 18% to 75% after traumatic brain injury, and from 47% to 97% after brain tumours. Fatigue is associated with factors including female sex, advanced age, dysfunctional families, history of specific health conditions, functional status (eg, fatigue prior to injury), comorbidities, mood, secondary disability, and the use of certain drugs. Assessment of fatigue is fundamentally based on such scales as the Fatigue Severity Scale (FSS). Advances have recently been made in imaging techniques for its diagnosis, such as in functional MRI. Regarding treatment, no specific pharmacological treatment currently exists; however, positive results have been reported for some conventional neurorehabilitation therapies, such as bright light therapy, neurofeedback, electrical stimulation, and transcranial magnetic stimulation. This review aims to assist neurorehabilitation professionals to recognise modifiable factors associated with fatigue and to describe the treatments available to reduce its negative effect on patients. Resumen: La fatiga es un síndrome multidimensional, complejo y frecuente en los pacientes con daño cerebral sobrevenido, influyendo negativamente en el proceso de neurorrehabilitación. Aparece desde etapas tempranas luego de la lesión y puede permanecer en el tiempo, recuperadas o no las secuelas del daño. La fatiga depende de circuitos neuronales superiores y se define como una percepción anómala de sobreesfuerzo. Tiene una prevalencia de 29% a 77% tras el ictus, 18% a 75% tras el traumatismo craneoencefálico (TCE) y 47% a 97% tras tumores cerebrales. La fatiga se asocia a factores como sexo femenino, edad avanzada, familia disfuncional, antecedentes patológicos específicos, estado funcional (p. ej. fatiga previa a la lesión), comorbilidades, estado anímico, discapacidad secundaria y uso de ciertos fármacos. Su estudio se realiza sobre todo a partir de escalas como la Escala de severidad de fatiga (Fatigue Severity Scale). Hoy en día existen avances en herramientas de imagen para su diagnóstico como la resonancia magnética funcional. En cuanto a su tratamiento, no existe aún terapia farmacológica definitiva, sin embargo, existen resultados positivos con terapias dentro de la neurorrehabilitación convencional, terapia lumínica y el uso del neurofeedback, estimulación eléctrica y magnética transcraneal. Esta revisión tiene como objetivo ayudar al profesional dedicado a la neurorrehabilitación a reconocer factores asociados modificables, así como terapias a su alcance para disminuir sus efectos nocivos en el paciente.

This manuscript presents a narrative review aimed at characterizing encephalopathy caused by beta-lactams, including its clinical presentation, diagnostic work-up, and therapeutic management. A systematic search was conducted using the PubMed, UpToDate, and StatPearls databases. The review included a range of studies, such as systematic reviews, observational studies, case series, and case reports, all of which examined the relationship between encephalopathy, beta-lactams, and neurotoxicity. Encephalopathy is a disorder of generalized attention, cognition, or consciousness, and its acute form can manifest with a wide range of symptoms, from mild confusion to delirium or coma. One possible cause of encephalopathy is the use of antibiotics, particularly beta-lactams. Neurotoxicity induced by beta-lactams presents with a rapid onset of symptoms within days, including myoclonus or seizures, abnormal electroencephalogram findings, and a normal magnetic resonance imaging scan. Treatment involves discontinuing the offending drug, which leads to a resolution of symptoms within a few days. This review underscores the importance of conducting more comprehensive studies with clearly defined inclusion criteria in order to improve the understanding and diagnosis of this condition. [ABSTRACT FROM AUTHOR]

The claustrum sign is a neuroimaging sign that has been described as hyperintense areas that are observed in magnetic resonance imaging (MRI), in our patient it was also identified in computed tomography (CT) as hypodense areas in both claustrum. This sign has been reported in disorders associated with cytokine storms, such as COVID-19 encephalopathy, and may represent a cytokine-mediated neuroinflammation's specific marker. It is reported a case of an 8-year-old boy with COVID-19 who presented the claustrum sign, identified in CT and MRI. [ABSTRACT FROM AUTHOR]

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Copyright of Colombian Journal of Nephrology / Revista Colombiana de Nefrología is the property of Colombian Association of Nephrology & Hypertension and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introducción: el síndrome de Leigh (SL) es una enfermedad neurodegenerativa infrecuente que afecta principalmente a lactantes y a escolares, ocasionada por una mutación en genes involucrados en la vía de la fosforilación oxidativa y cuyo déficit produce una disfunción en el metabolismo energético mitocondrial. Clínicamente, se caracteriza por un rápido deterioro neurológico, hallazgos típicos en neuroimagen y marcadores bioquímicos que orientan en su reconocimiento. En la mayoría de los pacientes tiene un curso progresivo y mortalidad temprana. Presentación del caso: se presenta el caso de una lactante de 5 meses que presenta perdida de los hitos del desarrollo. Los paraclínicos mostraron lactoacidosis, en neuroimagen necrosis nucleobasal, y la secuenciación genómica completa puso en evidencia una mutación homocigota del gen nuclear mitocondrial de la enzima 3-hidroxiisobutiril-CoA hidrolasa HIBCH. La paciente evolucionó con epilepsia refractaria, movimientos anormales, síndrome de West, apneas y falleció a los 10 meses de vida por insuficiencia respiratoria aguda. Discusión: el SL es con frecuencia una enfermedad rápidamente progresiva, que puede ser causada por errores innatos del metabolismo como la mutación del gen de la enzima HIBCH. El diagnóstico confirmatorio se hace con secuenciación exómica o genómica masiva y su manejo consiste en el tratamiento de los síntomas, modificaciones nutricionales, cuidado paliativo y consejería genético-reproductiva. Conclusión: el SL por mutaciones en el gen HIBCH es una enfermedad neurodegenerativa con síntomas variables, que afecta el desarrollo motor e intelectual. El diagnóstico se basa en biología molecular. El tratamiento actual busca aliviar síntomas y ajustar la nutrición, evidenciando desafíos inherentes a errores innatos del metabolismo.

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Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

INTRODUCCIÓN: la encefalopatía posterior reversible es un síndrome clínico-imaginológico de inicio agudo o subagudo, que cursa con cefalea, alteración de conciencia, cambios visuales, convulsiones y signos neurológicos focales, relacionado con lesiones cerebrales de predominio parieto-occipital bilaterales y simétricas de aspecto hipodenso en la TAC de cráneo e hiperintenso en el T2 de la RM cerebral. Se asocia con hipertensión arterial aguda y con el uso de medicamentos inmunosupresores. OBJETIVO: presentar los casos del síndrome de encefalopatía posterior reversible identificados en el Hospital Universitario Erasmo Meoz de Cúcuta. MATERIAL Y MÉTODOS: se revisaron las historias clínicas de nueve pacientes estudiados en un período de 31 meses. RESULTADOS: de los nueve pacientes, seis tenían eclampsia, dos enfermedad crónica subyacente asociada a alteración renal y uno síndrome nefrítico. Todos presentaron hipertensión arterial, siete cefalea, seis cambios de conciencia, cinco alteraciones visuales, dos náuseas y vómito, uno focalización neurológica, uno alucinaciones visuales y auditivas y uno confusión. Todos presentaron crisis epilépticas tónico-clónico generalizadas y uno de ellos estado epiléptico. Ocho tenían pruebas de función renal anormales. En la TAC de cráneo 8 pacientes tenían lesiones hipodensas corticosubcorticales y 1 subcorticales; las regiones parietooccipitales siempre estuvieron afectadas. Tres pacientes fallecieron (dos por complicaciones de sus patologías de base y uno por estado epiléptico), dos pacientes presentaron como secuela ceguera cortical y epilepsia, respectivamente. CONCLUSIONES: el síndrome de encefalopatía posterior reversible es frecuente en nuestro medio y obedece a múltiples causas. El tratamiento temprano de sus factores desencadenantes puede prevenir el infarto cerebral. Este consiste en la rápida corrección de las cifras tensionales elevadas, la suspensión de medicaciones asociadas con el síndrome y el tratamiento de aquellas enfermedades que favorecen su aparición (Acta Neurol Colomb 2005;21:289-298).

Introduction: the methyl-CpG binding protein 2 (MECP2) gene is located on chromosome Xq28; Rett syndrome (RS) occurs when there is a mutation in this gene. RS predominantly affects women; however, it can also occur in men. Objective: to describe the clinical characteristics of a male patient with RS. Presentation of case: seven-month-old male patient, who had seizures since birth. At four months he presented neurodevelopmental regression, choreodysonic movements, lack of head growth, dysautonomic symptoms and alterations in respiratory pattern, all of which were suggestive of progressive encephalopathy. Metabolic and infectious etiologies were ruled out. The genetic study revealed pathogenic variant c.806del (p.Gly269Alafs*20) in MECP2, confirming the diagnosis of SR. The patient continued to deteriorate until he died. Conclusion: RS in men has a more unfavorable prognosis than women, but the clinical characteristics are similar. [ABSTRACT FROM AUTHOR]

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El trasplante de órganos es una alternativa terapéutica cada vez más frecuente en nuestro medio y con ello las complicaciones y efectos de las medicaciones inmunosupresoras que afectan el sistema nervioso central (SNC). El síndrome de encefalopatía posterior reversible (SEPR) es un trastorno caracterizado por manifestaciones neurológicas potencialmente reversibles, asociadas a cambios en las neuroimágenes, en estrecha asociación con factores precipitantes, dentro de los cuales, se destacan el uso de medicamentos inmunosupresores, quimioterapéuticos y algunas condiciones médicas como hipertensión arterial y enfermedades renales. Las características clinico-radiológicas de este trastorno usualmente revierten con la suspensión de los factores precipitantes; sin embargo el diagnóstico tardío puede llevar a un desenlace fatal. Se presenta un caso de SEPR en una paciente joven a quien se le realizó trasplante cardiaco de urgencia. Durante su manejo post-operatorio recibió tacrolimus como parte del tratamiento del paciente trasplantado. En la cuarta semana de post-operatorio y quinto día de tratamiento con tacrolimus desarrolló cefalea asociada a cifras tensionales elevadas, deterioro de la conciencia y episodios convulsivos tónico-clónicos generalizados; las manifestaciones neurológicas revirtieron en las 48 horas siguientes al retiro del tacrolimus, al igual que los cambios en las neuroimagenes que resolvieron un mes después de las manifestaciones iniciales.

Introduction: We do not have population data in Spain on the application of therapeutic hypothermia (TH). The objective was to examine adherence to management standards during TH of infants with hypoxic-ischemic encephalopathy (HIE). Method: Multicenter observational cohort study from the beginning of TH (year 2010) in 5 hospitals in a Spanish region, until year 2019. Results: 133 patients were recruited, 72% diagnosed with moderate HIE and the rest of them with severe HIE. In 84% of infants, passive hypothermia was started at birth. Active TH was started at a median age of 5 h of life (IQR 3.3; 6.3), although the central targeted temperature (33−34 °C) was reached at a median age of 3.5 h (IQR 1; 6). Those born extramural, initiated active TH 3.3 h on average later than those born intramural, but without differences in the age at which the targeted temperature was reached.Sedoanalgesia was used in 97%. 100% were monitored with amplitude-integrated EEG and 59% with cerebral oxymetry. MRI was performed in 94% with moderate HIE vs. 65% with severe; P

Introduction: Liver transplantation is the only curative treatment for patients with end-stage liver disease. Neurological complications are one of the main causes of morbidity and mortality. Objective: To study neurological complications after liver transplantation in paediatric patients. Methods: We conducted a retrospective study, including all paediatric patients younger than 17 years undergoing liver transplantation over a 12-year period at our centre. Results: Forty-six liver transplantations were performed in 38 patients. The most common indication was biliary atresia. Up to one-third of patients presented neurological complications, with psychomotor agitation being the most frequent. Incidence of neurological complications was significantly higher in the group of infants than in older age groups. Encephalopathy was more common in patients with acute liver failure than in those with chronic liver failure. Conclusions: Neurological complications, and particularly psychomotor agitation, are common after liver transplantation in paediatric patients. Resumen: Introducción: El trasplante hepático (TH) es el único tratamiento curativo para enfermos en situación de fallo hepático terminal. Las complicaciones eurológicas (CN) son una causa importante de morbimortalidad. Objetivos: Estudiar la incidencia de CN en pacientes pediátricos sometidos a un TH. Pacientes y métodos: Estudio retrospectivo en el que se incluyeron todos los pacientes menores de 17 años sometidos a TH durante un periodo de 12 años. Resultados: Se realizaron 46 TH en 38 pacientes. La indicación más frecuente fue la atresia de vías biliares. En un tercio de los pacientes hubo alguna CN, siendo la más frecuente la agitación psicomotora. Se encontró una menor incidencia de CN en el grupo de lactantes con respecto a los pacientes de mayor edad, de forma estadísticamente significativa. El desarrollo de encefalopatía en casos de fallo hepático agudo fue más frecuente que en aquellos con insuficiencia hepática crónica. Conclusiones: Las CN en los niños son frecuentes después de un TH, siendo la más frecuente la agitación psicomotora.

Las encefalopatías tóxicas pueden ser causadas por una gran variedad de xenobióticos por mecanismos directos e indirectos simulando enfermedades metabólicas autoinmunes o neoplásicas. Por ende, requieren un anamnesis adecuada, un examen físico amplio y en cuanto a lo toxicológico tratar siempre de encontrar un nexo epidemiológico. Dentro de las principales causas están psicofármacos y drogas de abuso. El reconocimiento temprano de una encefalopatía tóxica es fundamental entendiendo que llevará al retiro de la noxa, inicio de manejo disminuyendo complicaciones y mortalidad asociada. Se describe el caso de una paciente co ingesta de ácido valproico quien presentó una encefalopatía por este anticonvulsivante sin compromiso de enzimas hepáticas, con alteraciones en el electroencefalograma que revirtieron por completo con la suspensión del medicamento. La importancia de este caso está en reconocer al ácido valproico como una causa de encefalopatía.

Introdução: Evidências experimentais, assim como estudos clínicos, sugerem a redução da lesão cerebral e melhora do desfecho neurológico, em recém-nascidos com encefalopatia isquêmica hipóxica (EHI) submetidos à hipotermia terapêutica (HT). Objetivo: Verificar a potencialidade da terapia hipotérmica de encefalopatia hipóxico-isquêmica (EHI) na asfixia neonatal, com base em dados da literatura, comparando os benefícios entre o resfriamento seletivo da cabeça (RSC) e o resfriamento de corpo inteiro (RCI), visto que o uso de hipotermia terapêutica (HT) como tratamento padrão em recém-nascidos com EHI moderada ou grave tem sido amplamente adotada. Métodos: Foi realizada uma busca nas bases de dados PubMed e SciELO de estudos em humanos, utilizando-se as palavras-chave “Therapeutic Hypothermia”, “Induced Hypothermia”, “Hypoxic-Ischemic Encephalopathy”, “selective head cooling”, “whole body cooling” e suas respectivas variáveis. Resultados: Foram selecionados 11 artigos para compor a revisão, após leitura detalhada. É consenso, a redução do risco de morte ou incapacidade aos 18 meses de vida nos neonatos com EHI moderado a grave, submetidos à HT através das técnicas de RCI ou RSC. Constatou-se diante dos estudos que não há diferença em termos de efeitos adversos entre os dois métodos. Quanto às alterações radiológicas, as lesões hipóxico-isquêmicas e incidência de convulsões após o resfriamento são mais frequentes com o RSC. Conclusão: Tanto RCI quanto o RSC demonstraram propriedades neuroprotetoras, embora o RCI proporcione uma área de proteção cerebral mais ampla. No entanto, não foram constatadas diferenças significativas entre os métodos quanto a efeitos adversos e a resultados benéficos em curto e longo prazo.

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Gastrointestinal infection usually manifests with nausea, vomit and abdominal pain, all of them wit course and variable severity. Extrainstestinal compromise is described, even without gastrointestinal symptoms, what causes a delay on diagnosis and treatment, worsening the prognosis. Ekiri syndrome, also known as lethal toxic encephalopathy is characterized by an acute neurological dysfunction secondary to enterobacterial infection which favor thrombi development and local inflammation mediated by tumor necrosis factor alpha and IL-1β with blood brain barrier dysfunction and high mortality. As we know, we present the first Ekiri syndrome case reported in Colombia.

Introduction: Triphasic waves (TW) constitute an electroencephalographic pattern associated with certain kinds of encephalopathy. Brain atrophy may be a predisposing factor linked with TW. Objective: To compare the degree of brain atrophy and white matter disease between patients with acute encephalopathy with and without TW. Methods: A retrospective observational study including adult patients with encephalopathy, with and without TW, hospitalized between 2016 and 2017. The degree of brain atrophy and white matter lesion were defined using the Global Cortical Atrophy and Age Related White Matter Changes (ARWMC) scales, respectively. Scores were compared between groups. Mortality rates were registered. Results: Sixteen patients with TW were identified matched by age and sex with 30 patients without TW. The mean age was 80 years in the TW group. Women represented 87.5%. Multifactorial encephalopathy was the most frequent diagnosis followed by metabolic encephalopathy. Patients with TW had more brain atrophy (10.43 vs 6.9, p= 0.03). Mean ARWMC was 9.43±6.5 and 8.5 ±7.89 in patients with and without TW respectively (p= 0.5). Mortality rate was higher in the TW group (31.25 vs 6.66% p= 0.02). Conclusions: Patients with acute encephalopathy and TW had higher degree of cerebral atrophy. It is possible that this structural alteration predisposes to the appearance of TW. There was no significant difference in white matter lesion degree. The mortality of the TW group was high, so future studies are necessary to determine their prognostic value. [ABSTRACT FROM AUTHOR]

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Introduction: The acute liver failure is an entity of multifactorial origin that is presented in previously healthy children and has direct repercussion in the synthesis, clotting and purification functions. Objective: To characterize children with acute liver failure according to clinical and humoral variables. Methods: A retrospective and descriptive study of 19 patients with diagnosis of acute liver failure was carried out, they were assisted in the Pediatric Intensive Cares Unit of the Southern Children Hospital in Santiago de Cuba, from April, 1998 to the same month in 2018, for which theoretical and statistical methods were used. Results: In the case material there was a prevalence of the female sex (57.9 %), the mean age was 5 years and the infection constituted the most common cause (73.7 %). The hepatotropic virus as the hepatitis A were the most frequent. The complications of more observance were the respiratory alkalosis (63.1 %), the multiorganic dysfunction (42.1 %) and the liver brain disease (31.6 %). The low figures of cholesterol and the prothrombin time higher than 20 seconds were associated with a greater lethality. Conclusions: In the patients younger than one year the non hepatotropic virus constituted the most frequent origin in this disease.

Posterior reversible encephalopathy syndrome constitutes a transient clinical and radiological entity, with multiple risk factors in which endothelial injury and compromise in cerebral perfusion are the common characteristics. Brain magnetic resonance is the method of choice for diagnosis. This is the case of a 26-year-old woman with a personal history of apparent health, who after an eutocic delivery suffered hypovolemic shock, product of postpartum hemorrhage due to uterine atony resulting in subtotal obstetric hysterectomy, mechanical ventilation with triple vasoactive support; after a favorable progress, she began with severe headache and visual disorders, high blood pressure and presented two episodes of generalized tonic-clonic seizures. A skull/brain CT scan of was performed and brain magnetic resonance study was also requested. The case is presented because of the unusual nature of this type of entity in everyday medical practice.

Introducción: El virus SARS-CoV-2, responsable de la COVID-19 presenta una alta tasa de contagio y es capaz de producir afecciones a diferentes niveles en el organismo, e incluye el sistema nervioso central, con manifestaciones como crisis convulsiva febril y afebril, estado de mal epiléptico, encefalopatías y encefalitis. Objetivo: Describir un paciente con encefalopatía, como forma de presentación de la COVID-19. Caso clínico: Paciente de 25 años con antecedentes de hidrocefalia obstructiva postraumática, con derivación ventrículo - peritoneal, positivo a la COVID-19, quien desarrolló manifestaciones neurológicas, en ausencia de manifestaciones respiratorias. Fue tratado según el protocolo para pacientes con la COVID-19, medidas antiedema cerebral y uso del péptido CIGB-258. Tuvo una evolución favorable hacia la recuperación. Conclusiones: En pacientes con encefalopatía de causa desconocida, en el contexto de la pandemia por la COVID-19, debe considerarse la infección por SARS-CoV-2. La evolución puede ser favorable con el uso de medidas generales y antiedema cerebral.

We present a unique clinical case of venous congestive encephalopathy in the context of a cerebral arteriovenous fistula with clinical worsening secondary to valvular overdrainage. ICP monitoring, the different pressure settings of the programable CSF shunt and the detailed clinical description that is carried out offer us enough data to understand that this case provides important pathophysiological knowledge to a little-known disease., (Copyright © 2024 Sociedad Española de Neurocirugía. Published by Elsevier España, S.L.U. All rights reserved.)

Contrast-induced encephalopathy is a neurological complication related to contrast used in endovascular procedures or computed tomography (CT). The main risk factors are arterial hypertension, diabetes mellitus, chronic kidney disease (CKD), hyperosmolar contrasts, the amount of infused contrast and its direct infusion in the posterior cerebral territory, or pathologies with blood-brain barrier damage. Symptomatology is non-specific and may present as altered level of consciousness, neurological focality or seizures. Diagnosis is done by exclusion after ischemic or hemorrhagic stroke has been ruled out; CT or MRI are useful for differentiation. Generally, it appears shortly after exposure and the symptoms lasts 48-72h with complete recovery, although cases with persistence of symptoms or longer duration have been described. Treatment consists of monitoring, supportive measures and kidney replacement therapy (KRT) with hemodialysis (HD) in patients in chronic KRT program. It is important for the nephrologist to be aware of this entity given the susceptibility of the patient on HD as well as its potential therapeutic role in these patients., (Copyright © 2023 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Copyright of Ginecología y Obstetricia de México is the property of Federacion Mexicana de Ginecologia y Obstetricia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

La hiperamonemia es una condición frecuente en pacientes cirróticos y en el contexto de una causa no cirrótica se relaciona con aumento en la producción de amonio o alteración en su eliminación. La presentación clínica de esta condición es inespecífica: va desde alteración del comportamiento hasta estado de coma, siendo una de las causas de diálisis no renal por determinados valores o refractariedad a manejo médico. Se presenta el caso de una mujer de 35 años, quien ingresó al servicio de urgencias con alteración del estado de conciencia, niveles de amonio elevados y masa hipervascular en hígado. Los estudios de aminoácidos limitantes del ciclo de la urea y ácido orótico urinario fueron normales y la biopsia de la lesión hepática reportó carcinoma hepático fibrolamelar, al cual se atribuyó la presencia de shunt portosistémico que causaba la hiperamonemia. Se indicó diálisis por persistencia de elevaciones de amonio y poca respuesta al tratamiento médico. Dada la evolución de la paciente, fue necesario reiniciar la terapia reemplazo renal por reaparición de estado encefalopático al suspender la misma. Esta terapia se mantuvo hasta el trasplante hepático que se realizó como tratamiento del carcinoma, con posterior estabilización de niveles de amonio y suspensión de la diálisis.

Fatigue is a complex, multidimensional syndrome that is prevalent in patients with acquired brain damage and has a negative impact on the neurorehabilitation process. It presents from early stages after the injury, and may persist over time, regardless of whether sequelae have resolved. Fatigue is conditioned by upper neuronal circuits, and is defined as an abnormal perception of overexertion. Its prevalence ranges from 29% to 77% after stroke, from 18% to 75% after traumatic brain injury, and from 47% to 97% after brain tumours. Fatigue is associated with factors including female sex, advanced age, dysfunctional families, history of specific health conditions, functional status (eg, fatigue prior to injury), comorbidities, mood, secondary disability, and the use of certain drugs. Assessment of fatigue is fundamentally based on such scales as the Fatigue Severity Scale (FSS). Advances have recently been made in imaging techniques for its diagnosis, such as in functional MRI. Regarding treatment, no specific pharmacological treatment currently exists; however, positive results have been reported for some conventional neurorehabilitation therapies, such as bright light therapy, neurofeedback, electrical stimulation, and transcranial magnetic stimulation. This review aims to assist neurorehabilitation professionals to recognise modifiable factors associated with fatigue and to describe the treatments available to reduce its negative effect on patients., (Copyright © 2024 Sociedad Española de Neurología. Published by Elsevier España, S.L.U. All rights reserved.)

Introduction: Introduction: the vitamin cobalamin is essential for a proper functioning of the CNS, hematopoiesis, and DNA synthesis. Its deficiency is frequently secondary to pernicious anemia or strict vegetarian diets. Case report: an 18-month-old male infant presented with a decreased level of consciousness and movement disorder (tremor and choreiform movements) of several hours' standing. He had a history of delayed acquisition of motor milestones (not standing, monosyllabic language), and progressive loss of these over the last few weeks (head support and sitting). He had been breastfed from birth. His family has a vegetarian diet. In neuroimages, cranial CT and MRI scans showed generalized supratentorial atrophy involving both matters and the basal ganglia. Treatment was started with intramuscular vitamin B12, which increased its levels. Subsequently, the patient was subjected to dietary diversification and oral cyanocobalamin, with clinical normalization after 6 months and radiological normalization after 7 months. Conclusions: we emphasize the importance of vitamin B12 supplementation during pregnancy and lactation in vegetarina mothers and their infants. [ABSTRACT FROM AUTHOR]

Objetivo: La cirrosis hepática ocasiona significativa mortalidad y morbilidad. Esta investigación trata de determinar la presentación clínica, la etiología y las complicaciones de los pacientes con cirrosis hepática en una población que habita en una región de altura del Perú. Materiales y métodos: Evaluación retrospectiva de la presentación clínica y las complicaciones de la cirrosis hepática. Se estudiaron 108 historias clínicas de pacientes cirróticos ingresados en el Servicio de Medicina del Hospital Nacional Ramiro Prialé Prialé de la ciudad de Huancayo entre el 2010 y el 2012. Resultados: El promedio de edad de los pacientes fue de 60,50 años (rango 12-82 años) y el 62,90 % fueron varones. La etiología más frecuente fue la ingesta alcohólica (63,00 %) seguida por las hepatitis B y C crónicas (7,40 % y 2,80 %, respectivamente). El 58,30 % de los casos correspondía al estadio B de la clasificación de Child-Pugh y el 31,30 % se encontraba en estadio C. La manifestación clínica más frecuente fue la distensión abdominal (87,00 %). Las complicaciones más comunes fueron la ascitis (56,00 %), la encefalopatía hepática (47,20 %) y el síndrome hepatorrenal (8,30 %). Conclusiones: La cirrosis alcohólica fue la etiología más común y las complicaciones más frecuentes fueron la ascitis y la encefalopatía hepática.

Copyright of Revista de Gastroenterología del Perú is the property of Sociedad de Gastroenterologia del Peru and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: The acute liver failure is an entity of multifactorial origin that is presented in previously healthy children and has direct repercussion in the synthesis, clotting and purification functions. Objective: To characterize children with acute liver failure according to clinical and humoral variables. Methods: A retrospective and descriptive study of 19 patients with diagnosis of acute liver failure was carried out, they were assisted in the Pediatric Intensive Cares Unit of the Southern Children Hospital in Santiago de Cuba, from April, 1998 to the same month in 2018, for which theoretical and statistical methods were used. Results: In the case material there was a prevalence of the female sex (57.9 %), the mean age was 5 years and the infection constituted the most common cause (73.7 %). The hepatotropic virus as the hepatitis A were the most frequent. The complications of more observance were the respiratory alkalosis (63.1 %), the multiorganic dysfunction (42.1 %) and the liver brain disease (31.6 %). The low figures of cholesterol and the prothrombin time higher than 20 seconds were associated with a greater lethality. Conclusions: In the patients younger than one year the non hepatotropic virus constituted the most frequent origin in this disease. [ABSTRACT FROM AUTHOR]

Copyright of Current Neurology / Aktualno?ci Neurologiczne is the property of Medical Communications Sp. z o.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: CADASIL (Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is an autosomal dominant neurovascular disorder that causes ischemic subcortical stroke, migraine with aura, depression, apathy, and dementia. It have a variable prevalence (at least 2-10.7 per 100,000 adults) and is the most common cause of inherited stroke and vascular dementia in adults. Clinical case: Female patient aged 44 with a history of migraine with aura since age 25. Also, family history of migraine, stroke, death and disability in youngsters. She arrives with clinical picture of acute encephalopathy that begins with a migraine headache accompanied by vomiting, photophobia, scotoma and later fever and hallucinations. Brain MRI shows abnormalities such as several lacunar infarcts and T2 hyperintensities involving the white matter of the left anterior temporal pole. The EEG shows slow background. Diagnosis was confirmed with detection of eosinophilic inclusions in smooth muscle cell of dermic capillary of skin biopsy (osmophilic in transmission electronic microscopy). Conclusions: The patient showed is the first confirmed case in Cuba with CADASIL. Unfortunately, because of similarities in clinical presentation and neuroimaging, this disorder is often misdiagnosed as multiple sclerosis and treated with immunomodulatory medications that confer risk without benefit. [ABSTRACT FROM AUTHOR]

Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Liver transplant is a definitive treatment of end-stage liver insufficiency. The clinical state and biochemical parameters used for grading liver insufficiency can influence the functioning of the coagulation system and the amount of intraoperative blood loss. Aim of the study: The aim of the study was to assess the influence of the clinical state and stage of liver insufficiency on blood loss during liver transplantation. Material and methods: The study included 88 patients aged 19-67 years after liver transplantation at the Independent Public Regional Integrated Hospital in Szczecin, Poland. A retrospective analysis was carried out of data collected from liver transplantation qualification protocols, which contained social-demographic and epidemiological information. Results: Average blood loss during liver transplantation amounted to 3082 ±2708 ml (range 400-16,000 ml). The average total surgery time was 371.21 min (range 255-405 min). Blood loss correlated with the model for end stage liver disease (MELD) and Child-Turcotte-Pugh score (CTP) values. However, an independent relationship with the amount of intraoperative blood loss was confirmed in the discriminant analysis only for three parameters, namely encephalopathy (p = 0.0032), poor dietary habits (p = 0.00107), and surgery duration (p = 0.00178). Conclusions: Cachexia and encephalopathy constitute independent clinical factors of the increased risk of intraoperative bleeding. Surgery duration is an independent factor conditioning the amount of intraoperative blood loss. [ABSTRACT FROM AUTHOR]

Copyright of Revista Médica Clínica Las Condes is the property of Editorial Sanchez y Barcelo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Sepsis associated delirium (SAD) is defined as diffuse brain damage caused by a systemic inflammatory response to infection, but without signs of central nervous system infection. This term replaced the term "septic associated encephalopathy" (SAE) used previously. The occurrence of ICU delirium in critically ill patients treated for generalized infection is associated with prolonged mechanical ventilation, time of hospitalization, long-term functional and cognitive impairment. A large amount of clinical data and research in the field of basic sciences indicate that inflammation of the nervous tissue, abnormal cerebral perfusion and disturbances in the balance of neurotransmitters are the main mechanisms underlying the development of SAD. There are no laboratory or electrophysiological tests or imaging studies or SAD-specific therapies, but this syndrome usually disappears after successful treatment of sepsis. After stabilizing the patient's condition, providing respiratory, cardiovascular and other organ support, and implementing effective treatment of infection, patients with severe sepsis or septic shock should undergo motor and cognitive rehabilitation as soon as possible because early onset may shorten the duration of the delirium. After establishing reliable and consistent definitions of SAD, it is necessary to conduct further studies explaining the pathophysiology of this condition and to develop dedicated methods of treatment. [ABSTRACT FROM AUTHOR]

Background. Craniofacial injuries require highly specialized interdisciplinary treatment and qualified care. Adequate therapy aims to minimize unfavorable phenomena that develop following an injury. Properly conducted treatment translates into the patient's functioning in the future and his quality of life after returning to society. The final result of the treatment depends on many processes responsible for damage to the central nervous system as opea result of the injury and after it. They include neurotransmission disorders, the effect of inflammatory response markers and cytokines on the activation of specific nervous system structures and neurodegenerative processes. Case report. In this paper, the case of a patient hospitalized in the Department of Anesthesiology and Intensive Care presents an analysis of possible causes of neurocognitive disorders and disorders in social functioning. [ABSTRACT FROM AUTHOR]

Introducción: La edad materna avanzada se ha asociado con un aumento en el riesgo de morbimortalidad perinatal. Conocer los factores asociados ayudará a tomar las decisiones médicas correctas sobre cada paciente y disminuir las complicaciones. Objetivo: Evaluar la morbilidad asociada con la edad materna avanzada en los recién nacidos pretérmino ingresados a la UCIN del Hospital Español de México. Material y métodos: Estudio observacional, descriptivo, retrospectivo que incluyó a todos los recién nacidos pretérmino ingresados a la UCIN entre marzo de 2014 y septiembre de 2016. Se registró género, edad gestacional, peso, días de estancia y diagnósticos de egreso. Resultados: Se obtuvieron 460 recién nacidos pretérmino, 258 (56.1%) fueron hijos de madres de edad avanzada. Se encontraron resultados significativos al analizar la prevalencia de enfermedad hipóxico-isquémica y enterocolitis necrosante, y mayor frecuencia de patologías como broncodisplasia, apneas del prematuro, cardiopatías congénitas, restricción del crecimiento intrauterino y trisomía 21. La mortalidad global fue del 5.6%; 2.4% corresponde a recién nacidos pretérmino con antecedente de edad materna avanzada. Conclusiones: Los resultados obtenidos son importantes, pues hasta el momento la complicación asociada con la edad materna avanzada más estudiada ha sido el riesgo de premadurez, y en el caso de nuestro estudio la presencia de enterocolitis necrosante y enfermedad hipóxico-isquémica. Introduction: Advanced maternal age has been associated with an increased risk of perinatal morbidity and mortality. Knowing the associated factors will help make the right medical decisions about each patient and decrease the complications. Objective: To evaluate morbidity associated with advanced maternal age in preterm infants admitted to the NICU of the Hospital Español. Material and methods: An observational, descriptive, retrospective study that included all newborns who were admitted to the NICU between March 2014 to September 2016. Gender, gestational age, weight, days of stay and discharge diagnoses were recorded. Results: We obtained 460 preterm infants, 258 (56.1%) were children of elderly mothers. Significant results were seen when analyzing the prevalence of hypoxic-ischemic disease and necrotizing enterocolitis, and a greater frequency of pathologies such as bronchodysplasia, premature apnea, congenital heart disease, intrauterine growth restriction and trisomy 21. Overall mortality was 5.6%, 2.4% corresponds to preterm newborns with a history of advanced maternal age. Conclusions: The results obtained are important, because so far, the complication associated with advanced maternal age more studied has been the risk of prematurity, and in the case of our study the presence of necrotizing enterocolitis and hypoxic-ischemic disease. [ABSTRACT FROM AUTHOR]

Introduction: Susac's Syndrome (SS) is a rare disease first described in 1979 characterized by the clinical triad of encephalopathy, neurosensory auditory loss, and partial or complete occlusion of the retinal artery. Described as an inflammatory disease, presumably an autoimmune disease, against vascular endothelium that causes occlusion of the small vessels. The diagnosis is supported by brain MRI, retinal fluorography and audiometry. It's a subdiagnosed syndrome with numerous differential diagnostics. The prevalence is unknown, until now only 300 cases have been registered worldwide. Young women are the most affected. Case presentation: 34-year-old woman, no history of chronicdegenerative diseases, catholic, housekeeper, doesn't keep pets or other animals, no surgical history, no allergies, no use of tobacco, alcohol, or illicit drugs, no recent travels. Medical history: begins 6 months ago with vertigo, emesis of undigested food in multiple occasions, holocranial cephalalgia. After 2 months, presents sudden auditory loss, right ear tinnitus, somnolence, disorientation, difficulty articulating words, lower limbs weakness, and difficulty walking. PE: BP 100/60mmHg, HR 78', T 36.5°C, RR 15'; normocephalic, inexpressive face, skin and mucous membranes well hydrated and without pallor, no infiltration to subcutaneous cellular tissue, neck without jugular venous distention; at pulmonary level with vesicular murmur, no rales or wheezing, no pathological sounds; cardiac sounds with adequate tone and volume, no murmurs; abdomen soft, depressible, non painful, without signs of peritoneal irritation. At neurological level: awake, capable of fixating attention but for short periods of time, monotonous speech, comprehends simple commands but doesn't obeys them, uncooperative. Cranial nerves: I not assessable, II visual acuity not assessable, visual field campimetry indifferent, III IV and VI central primary gaze, isochoric pupils, normal photopupillary and consensual reflexes, rest of cranial nerves without alteration; strength 4/5 in upper limbs and 3/5 in lower limbs, normal sensory; cerebellum and gait not assessables; atavistic reflexes absent; no abnormal movements; meningeal signs absent. Fundoscopic exam is normal. CBC: WBC 6.7 Neut 5 Hb 13.1 Plat 264 Gluc 106 Urea 41 Cr 0.9 Na 136 K 4.1 Cl 101 BUN 20; CSF normal, CSF culture negative, CSF cytology normal; LFT with TB 0.9 CB 0.6 UB 0.3 ALT 25 AST 16. Cerebral MRI: periventricular white matter lesions, which are hyperintense in T2, with multiple small lesions in the central portion of the corpus callosum. Audiometry: right asymmetry in phonemic discrimination. Fluorescein angiography: hyperfluorescence of peripheral retinal arteries. Vestibular tests: no spontaneous nistagmus, right canalicular hypoexcitability of 26%, study compatible with vestibular dysfunction at brain stem level and right intracanalicular paresis. Medical treatment was indicated with human immunoglobulin for 5 days, with improvement of symptoms, mental functions and strength, remaining only with right hypoacusis. Control MRI with evidence of improvement with decrease of the hyperintense lesions, remaining only the lesions at the corpus callosum. Patient is discharged with ambulatory treatment. Differential diagnosis: Multiple Sclerosis, Optic Neuritis, Encephalitis, among others must be ruled out. Conclusion: SS is an infrequent entity, characterized by cerebral, retinal and auditory affection with multiple differentials, which make its diagnosis a medical challenge. [ABSTRACT FROM AUTHOR]

Susac's syndrome (RED-M, SICRET, retinocochlearcerebral vasculopathy) is a rare autoimmune disorder that belongs to systemic connective tissue diseases. The syndrome mainly affects young women aged 21 to 41 years; the female to male ratio is 3:1. The exact cause of the disease is still unknown although it has been hypothesized that some infectious or immune factors can contribute to its development (some patients have low-titer antinuclear antibody or rheumatoid factor tests; remission has been observed in patients receiving immunosuppressive therapy). Susac's syndrome commonly starts with central nervous system dysfunction followed by the triad of subacute encephalopathy, vision disorders and hearing loss. These signs do not necessarily develop simultaneously; furthermore, they may vary in severity. The diagnosis is typically made based on clinical symptoms, detailed ophthalmic examination and MRI findings. Due to its rare occurrence and unknown pathogenesis, no consistent recommendations have been developed regarding the treatment of Susac's syndrome. The disease is frequently self-limited and spontaneously remits after 2 to 4 years. The therapies include corticosteroids, immunosuppression (cyclophosphamide, azathioprine, mycophenylate mofetil, methotrexate, cyclosporin A), intravenous immunoglobulin, antiplatelet antithrombotic agents, hyperbaric oxygen and plasmapheresis. In patients who are unresponsive to standard therapy, infliximab or rituximab might be added. Numerous experts believe antiplatelet medication as well as vasorelaxants and vasodilators should be used as adjuvant treatment. Patients with severe hearing loss may benefit from cochlear implants. Intratympanic injections of dexamethasone have been administered in the acute phase of hearing loss and tinnitus. Treatment of migraine-like headaches includes naratriptan and topiramate while methylprednisolone pulse therapy is used to relieve generalized headaches. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos Brasileiros de Oftalmologia is the property of Arquivos Brasileiros de Oftalmologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)