ABSTRACT
Introducción: la necrosis laminar cortical es un término radiológico que describe la presencia de lesiones hiperdensas de localización cerebral, las cuales siguen una distribución giriforme y se observan con mayor sensibilidad en los estudios de resonancia magnética cerebral (RM). Esta condición patológica, que afecta a la corteza del cerebro, suele ser secundaria a una depleción de sus fuentes energéticas como consecuencia de hipoxia cerebral, alteraciones metabólicas, hipoglicemia, falla renal o hepática, intoxicaciones o infecciones. Presentación del caso: se reporta el caso de un hombre de 23 años, con antecedente de consumo crónico de alcohol, quien ingresó al servicio de urgencias de nuestra institución con un estado epiléptico. El estudio de resonancia magnética cerebral demostró la presencia de una necrosis laminar cortical con posterior déficit neurocognitivo y funcional. Conclusión: si se consideran las secuelas neurológicas potenciales asociadas a un estado epiléptico, relacionadas con necrosis laminar cortical cerebral, es necesario hacer un diagnóstico etiológico precoz, así como una atención terapéutica temprana a los pacientes.
Introduction: Cortical laminar necrosis (CLN) is radiologically defined as high-intensity cortical lesions on T1-weighted MRI images that follow a gyral distribution in the brain. Histopathologically, this pathological condition is characterized by necrosis of the cortex involving neurons, glial cells, and blood vessels. It is usually triggered by hypoxia, metabolic alterations, drugs, intoxications, or infections. Case description: We report the case of a 23-year-old man with a history of chronic alcohol abuse who was admitted to our institution with status epilepticus. The brain magnetic resonance imaging performed on this patient showed cortical laminar necrosis associated with subsequent neurocognitive deficits. Conclusion: Due to the potential neurological sequelae secondary to status epilepticus in relation to cortical laminar necrosis as permanent brain damage, it is necessary to provide early diagnosis and treatment for these patients.
Subject(s)
Status Epilepticus , Hypoxia, Brain , Cerebral Cortex , NeuroimagingABSTRACT
Abstract Anemia is associated with increased risk of Acute Kidney Injury (AKI), stroke and mortality in perioperative patients. We sought to understand the mechanism(s) by assessing the integrative physiological responses to anemia (kidney, brain), the degrees of anemia-induced tissue hypoxia, and associated biomarkers and physiological parameters. Experimental measurements demonstrate a linear relationship between blood Oxygen Content (CaO2) and renal microvascular PO2 (y = 0.30x + 6.9, r2= 0.75), demonstrating that renal hypoxia is proportional to the degree of anemia. This defines the kidney as a potential oxygen sensor during anemia. Further evidence of renal oxygen sensing is demonstrated by proportional increase in serum Erythropoietin (EPO) during anemia (y = 93.806*10−0.02, r2= 0.82). This data implicates systemic EPO levels as a biomarker of anemia-induced renal tissue hypoxia. By contrast, cerebral Oxygen Delivery (DO2) is defended by a profound proportional increase in Cerebral Blood Flow (CBF), minimizing tissue hypoxia in the brain, until more severe levels of anemia occur. We hypothesize that the kidney experiences profound early anemia-induced tissue hypoxia which contributes to adaptive mechanisms to preserve cerebral perfusion. At severe levels of anemia, renal hypoxia intensifies, and cerebral hypoxia occurs, possibly contributing to the mechanism(s) of AKI and stroke when adaptive mechanisms to preserve organ perfusion are overwhelmed. Clinical methods to detect renal tissue hypoxia (an early warning signal) and cerebral hypoxia (a later consequence of severe anemia) may inform clinical practice and support the assessment of clinical biomarkers (i.e., EPO) and physiological parameters (i.e., urinary PO2) of anemia-induced tissue hypoxia. This information may direct targeted treatment strategies to prevent adverse outcomes associated with anemia.
Subject(s)
Humans , Hypoxia, Brain/complications , Stroke , Acute Kidney Injury/etiology , Anemia/complications , Oxygen , Biomarkers , Kidney , Hypoxia/complicationsABSTRACT
RESUMEN Los sobrevivientes de la reanimación cardiopulmonar posterior a un paro cardiaco pueden tener un amplio rango de desenlaces y van desde recuperación neurológica completa, estado de vigilia sin respuesta, compromiso cognoscitivo diverso o la muerte. La lesión del tejido cerebral se presenta inmediatamente después del paro cardíaco, durante la reanimación y al retornar la circulación espontánea. La severidad y duración de la noxa isquémica determinarán el devenir neurológico. El examen clínico es el punto de partida en el abordaje multimodal del neuropronóstico. Se debe complementar con electroencefalograma, potenciales evocados somatosensoriales, neuroimágenes y biomar-cadores séricos. Entre un 10 a 15% de los pacientes con lesión cerebral posterior al paro cardiaco evolucionan hacia muerte por criterios neurológicos y son potenciales candidatos a la donación de órganos. Un retiro temprano de las terapias de sostenimiento de vida puede malograr la posibilidad de un potencial donante de órganos. Se puede estimar de manera temprana qué pacientes tienen mayor riesgo de evolucionar a muerte por criterios neurológicos. El neurólogo tiene un papel protagónico en el manejo de pacientes con lesión cerebral post paro cardiaco y sus decisiones tienen implicaciones éticas y legales.
ABSTRACT People who survive cardiopulmonary resuscitation (CPR) after cardiac arrest, have a wide range of outcomes including complete neurological recovery, coma, compromised cognitive function and death. Injury of the brain parenchyma starts immediately after a cardiac arrest, during CPR and return of spontaneous circulation. The severity of the ischemic injury will define the neurological outcome. The first step needed to determine a neurological prognosis is the clinical exam, with the help of electroencephalography, somatosensory evoked potentials, neuroimaging, and serum biomarkers. Between 10 and 15% of patients with brain injury after a cardiac arrest, develop brain death and become potential candidates for organ donation. A premature withdrawal of vital support can hamper the possibility of organ donation. The patients with higher risk of developing brain death can be identified early based on neurological criteria. The neurologist has a major role in the approach of patients with brain injury after cardiac arrest and the decision making with legal and ethical consequences.
Subject(s)
Brain Death , Hypoxia, Brain , Heart Arrest , Prognosis , EthicsABSTRACT
RESUMEN INTRODUCCIÓN: La leucoencefalopatia tóxica es una afección que compromete la sustancia blanca por exposición a sustancias tóxicas. La heroina es una de las implicadas en el desarrollo de la leucoencefalopatia con diferencias exclusivas que suceden con la inhalación según las diversas técnicas en comparación al uso intravenoso, bien sea de la heroína o de otras sustancias psicoactivas. En esta serie describimos cinco casos, de sexo masculino, que desarrollaron leucoencefalopatia espongiforme por heroína (LEH) posterior a la inhalación de vapores, en un hospital del sistema de salud público en la ciudad de Armenia, Colombia. OBJETIVO: El objetivo de este estudio es describir las características demográficas, clínicas, hallazgos de laboratorio e imágenes diagnósticas, así como la mortalidad asociada a LEH en la muestra estudiada. MÉTODOS: Recolección de datos de historias clinicas y búsqueda de imágenes registradas en el Hospital San Juan de Dios de Armenia durante el periodo 2017-2018. RESULTADOS: Se obtienen cinco casos clínicos de pacientes usuarios de vapores inhalados de heroina, quienes ingresan con signos neurológicos de predominio motores y extrapiramidales, con el signo radiológico clásico de "Chasing the Dragon" en estudios de TC cerebral simple en todos los casos. De los cinco casos se presenta un deceso, determinando una mortalidad de 20% comparado con un 25% de mortalidad reportado en la literatura. CONCLUSIONES: La LEH suele estar subdiagnosticada dado que suele confundirse con un trastorno neuropsiquiatríco o de la conducta asociada al consumo de sustancias psicoactivas (SPA), el diagnóstico se realizó con los hallazgos típicos en las imágenes de TC cerebral simple. Se debe tener en cuenta las estadísticas sobre consumo de heroína a la hora de realizar el abordaje de un paciente con historial de consumo de SPA y los signos neurológicos para relacionarlos con esta etiologia y dar un manejo integral a estos pacientes.
ABSTRACT IlNTRODUCTION: Toxic leukoencephalopathy is a condition that compromises the encephalic white matter due to exposure to toxic substances. Heroin is one of those involved in the development of leukoencephalopathy and there are certain differences that occur with its inhalation with the different techniques compared to intravenous use, either heroin or other psychoactive substances. In this serie, we describe five cases of male sex who developed heroin spongiform leukoencephalopathy (HSLE) after inhalation of vapors, in a Hospital of the public health system in the city of Armenia, Colombia. OBJECTIVES: The objective of this study is to describe the demographic and clinical characteristics, laboratory findings and diagnostic images, as well as the mortality associated with HSLE in the sample studied. METHODS: Collection of data from medical records and search of images registered at the San Juan de Dios Hospital in Armenia during the period 2017-2018. RESULTS: Five clinical cases were obtained of patients who were users of inhaled heroin vapors and were admitted to the hospital with predominantly motor and extrapyramidal neurological signs, with simple brain CT studies showing the classic radiological sign of "Chasing the Dragon" in all five cases. One death was presented, with a mortality of 20% compared to the 25% mortality that has been reported in the scientific literature. CONCLUSIONS: HSLE is usually underdiagnosed since it is often confused with a neuropsychiatric or behavioral disorder associated with the consumption of psychoactive substances (PAS). The diagnosis was made with the typical findings in simple brain CT images. Statistics on heroin use must be considered when approaching a patient with a history of PAS use and neurological signs, to relate them to this etiology and provide comprehensive management to these patients.
Subject(s)
Tomography, X-Ray Computed , Hypoxia, Brain , Inhalation , Heroin , LeukoencephalopathiesABSTRACT
Fundamento: O acidente vascular encefálico (AVE) é prevalente no mundo. Reconhecimento precoce da doença cardiovascular subclínica pode predizer um primeiro episódio de AVE isquêmico; o speckle tracking associado à ecocardiografia (STE) permite detecção precoce da disfunção miocárdica subclínica. Objetivo: Provar a associação entre deformação miocárdica avaliada pelo STE e primeiro episódio de AVE em indivíduos saudáveis. Método: Incluímos participantes entre 40-80 anos com primeiro episódio de AVE isquêmico sem cardiopatia conhecida, pareados por sexo, idade e hipertensão com grupo controle saudável na proporção 1:2. STE avaliou strain longitudinal (SL) do ventrículo esquerdo (VE), e ecocardiografia tradicional foi realizada. Análises univariada e multivariada avaliaram as relações do AVE com fatores de risco cardiovasculares e parâmetros derivados da ecocardiografia. Resultado: 29 casos e 62 controles foram incluídos. Média etária foi 60 ± 12 anos; 54% eram homens. Tabagismo foi mais prevalente em casos do que em controles (34% vs. 9%; p=0.001). Nenhum outro fator de risco evidenciou diferença estatística. Casos tiveram menor deformação miocárdica comparados aos controles (SL -16.7 ± 3.4% vs. -19.2 ± 2.8%; p < 0.001). Não houve diferença em relação aos parâmetros ecocardiográficos tradicionais. Após ajuste para tabagismo e hiperlipidemia, SL manteve-se independentemente associado com AVE (OR=1.3; 95% CI, 1.1 1.6; p=0.005). A área abaixo à curva ROC para AVE aumentou significativamente após adicionar SL ao tabagismo (0.65 para 0.78, respectivamente; p=0.009). Conclusão: SL tem independente associação com o primeiro episódio de AVE isquêmico em adultos de média idade com corações geralmente normais. SL pode ser potencial marcador de risco nesta população
Background: Stroke is prevalent worldwide, and early recognition of subclinical cardiovascular (CV) disease could predict a first ischemic stroke (IS) episode. Speckle-tracking echocardiography (STE) allows the detection of early subclinical myocardial dysfunction. Aim: To examine the association between myocardial deformation, evaluated by STE, and first episode of IS in a sample of otherwise healthy patients. Methods: We included individuals between 4080 years old, with a first incidence of IS, with no known CV disease, matched to healthy controls by sex, age, and hypertension at a 1:2 ratio. STE was used to assess LV global longitudinal strain (GLS), and traditional echocardiography was performed. Univariate and multivariable analyses were performed to assess the relationship among stroke, CV risk factors, and echocardiographyderived parameters. Results: A total of 29 cases and 62 controls were included. The mean age of the patients was 60 ± 12 y/o, and 54% were males. Smoking was more prevalent in cases compared to controls (34% vs. 9%; p = 0.001), and there were no significant differences in the other examined risk factors. Cases had less myocardial deformation compared to controls (GLS: -16.7% ± 3.4% vs. -19.2 ± 2.8%; p < 0.001), and there was no
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Cardiovascular Diseases/diagnostic imaging , Hypoxia, Brain/diagnostic imaging , Ventricular Dysfunction, Left/diagnostic imaging , Stroke/diagnostic imaging , Risk Factors , Longitudinal StudiesABSTRACT
La pseudohemorragia subaracnoidea es un fenoÌmeno infrecuente que se caracteriza por hallazgos sugestivos de hemorragia subaracnoidea en la tomografiÌa computarizada simple de craÌneo, sin evidencia de la misma en estudios adicionales. Se ha asociado a muÌltiples causas, de las cuales la principal es la encefalopatiÌa hipoÌxico-isqueÌmica posparo cardiaco y reanimacioÌn cardiopulmonar. El contexto cliÌnico y los niveles de atenuacioÌn medidos en Unidades Hounsfield (UH) se deben tener en cuenta al hacer el diagnoÌstico diferencial entre ambas entidades. Se presenta el caso de una paciente con pseudohemorragia subaracnoidea de etiologiÌa multifactorial.
Pseudo-subarachnoid hemorrhage (PSAH) is an infrequent entity characterized by findings in non- contrast head computed tomography that mimic subarachnoid hemorrhage, but without evidence of blood products in further studies. It has been associated with multiple etiologies, with hypoxic ischemic encephalopathy following cardiac arrest and cardiopulmonary resuscitation as the leading cause in literature. Clinical context and attenuation levels measured in Hounsfield Units should be taken into consideration when establishing the differential diagnosis between these entities. The case of a patient with PSAH of multifactorial etiology is presented.
Subject(s)
Subarachnoid Hemorrhage , Tomography, X-Ray Computed , Hypoxia, Brain , Meningitis, CryptococcalABSTRACT
BACKGROUND: Circular RNA (circRNA) is highly expressed in the brain tissue, but its molecular mechanism in cerebral ischemia-reperfusion remains unclear. Here, we explored the role and underlying mechanisms of circRNA antisense non-coding RNA in the INK4 locus (circ_ANRIL) in oxygen-glucose deprivation and reoxygenation (OGD/R)-induced cell injury. RESULTS: The expression of circ_ANRIL in OGD/R-induced human brain microvascular endothelial cells (HBMECs) was significantly up-regulated, while that of miR-622 was significantly down-regulated. Overexpression of circ_ANRIL significantly inhibited the proliferation of OGD/R-induced HBMECs and aggravated OGD/R-induced cell apoptosis. Moreover, circ_ANRIL overexpression further increased the secretion of interleukin (IL)-1ß, IL-6, tumor necrosis factor-a, and monocyte chemoattractant protein-1 in OGD/R-treated HBMECs. The results of bioinformatics analysis and luciferase reporter assay indicated that circ_ANRIL served as an miR-622 sponge to negatively regulate the expression of miR-622 in OGD/R-treated HBMECs. Additionally, circ_ANRIL silencing exerted anti-apoptotic and anti-inflammatory effects by positively regulating the expression of miR-622. Furthermore, inhibition of OGD/R-induced activation of the nuclear factor (NF)-kB pathway by circ_ANRIL silencing was significantly reversed by treatment with miR-622 inhibitor. CONCLUSIONS: Knockdown of circ_ANRIL improved OGD/R-induced cell damage, apoptosis, and inflammatory responses by inhibiting the NF-κB pathway through sponging miR-622.
Subject(s)
Humans , Reperfusion Injury/metabolism , Hypoxia, Brain/metabolism , MicroRNAs/physiology , MicroRNAs/genetics , RNA, Circular , Oxygen , Brain , Apoptosis , Cyclin-Dependent Kinase Inhibitor p16 , Endothelial Cells , RNA, Long Noncoding , Glucose/metabolism , InflammationABSTRACT
Introducción: Necrosis laminar cortical es un término imaginológico que se usa para describir lesiones de localización cortical, hiperdensas de distribución giriforme, en tomografía computarizada (TC). La etiología de este hallazgo involucra depleción de energía cerebral, la cual puede derivarse de múltiples patologías, que conllevan principalmente a hipoxia o alteraciones metabólicas. Presentación de caso: Es el caso de una paciente femenina de 3 meses de edad quien fue llevada a urgencias de la institución de los autores con un cuadro clínico de 1 semana de evolución consistente en elevación de la temperatura, disnea, cianosis, frialdad en extremidades, taquipnea, taquicardia y edema. Por medio de ecocardiografía se diagnosticó miocarditis de probable origen viral. Posteriormente, la paciente sufrió paro cardiorrespiratorio y choque prolongado que requirió reanimación cardiopulmonar e ingreso a UCI neonatal. Una TC cerebral tomada 1 semana después de estos eventos evidenció hallazgos compatibles con necrosis laminar cortical. Discusión: No hay descripciones epidemiológicas sobre este hallazgo; sin embargo, se ha teorizado un incremento en su frecuencia debido a la alta tasa de supervivencia de pacientes que padecen patologías hipóxico-isquémicas. A pesar de que los hallazgos de necrosis laminar cortical son descritos para la resonancia magnética (RM), también se pueden apreciar en la TC, donde típicamente se evidencian como una alta densidad cortical sutil, y los hallazgos más llamativos están relacionados con un peor pronóstico. Conclusión: Es necesaria la divulgación de este tipo de imágenes radiológicas, con el fin de promover la realización de pronósticos más acertados en pacientes en quienes se aprecien estos hallazgos.
Introduction: Cortical laminar necrosis is an imaging term used to describe gyriform hyperdense lesions in the cortical region that can be appreciated on the CT (Computed Tomography). The etiology of this finding involves brain energy depletion, which can be derived from multiple pathologies, that mainly lead to hypoxia or metabolic alterations. Case report: the case of a 3-month-old female patient is presented; she was taken to the emergency department with a 1-week clinical manifestations consisting of thermal rises, dyspnea, cyanosis coldness in extremities, tachypnea, tachycardia and edema. An echocardiography diagnosed myocarditis of probable viral origin. Subsequently, the patient presented cardiac arrest and prolonged shock that required cardiopulmonary resuscitation and admission to neonatal ICU. A cerebral CT scan taken 1 week after these events evidenced imaging findings compatible with cortical laminar necrosis. Discussion: There are no epidemiological descriptions of this finding, however, an increase has been theorized due to the high survival rates of patients suffering from ischemic hypoxic pathologies. Although findings of cortical laminar necrosis are typical of MRI, they can also be seen on CT scan, where they typically show as a subtle cortical hyperdensity, and the most striking findings are associated to a worst prognosis. Conclusion: Disclosure of these type of radiological images is necessary in order to promote more accurate prognoses in patients in whom these findings are appreciated.
Subject(s)
Cerebral Cortex , Tomography, X-Ray Computed , Hypoxia, Brain , NeuroimagingABSTRACT
Monitoring cerebral oxygenation using a near infrared spectroscopy (NIRS) device is useful for estimating cerebral hypoperfusion and is available during liver transplantation (LT). However, high serum bilirubin concentration can interfere with NIRS because bilirubin absorbs near infrared light. We report a patient who underwent LT with a diagnosis of vanishing bile duct syndrome, whose regional cerebral oxygen saturation (rSO₂) remained below 15% even with alert mental status and SpO2₂ value of 99%. The rSO₂ values were almost fixed at the lowest measurable level throughout the intra- and postoperative period. We report a case of erroneously low rSO₂ values during the perioperative period in a liver transplant recipient which might be attributable to skin pigmentation rather than higher serum bilirubin concentration.
Subject(s)
Humans , Bile Ducts , Bile , Bilirubin , Diagnosis , Hyperbilirubinemia , Hypoxia, Brain , Liver Transplantation , Liver , Oxygen , Perioperative Period , Postoperative Period , Skin Pigmentation , Spectrum Analysis , Transplant RecipientsABSTRACT
BACKGROUND: Pulmonary thromboembolism (PTE) is a life-threatening disease with high mortality. This study aimed to assess the outcomes of surgical embolectomy and to clarify the sustained long-term effects of surgery by comparing preoperative, postoperative, and long-term follow-up echocardiography outcomes. Of 22 survivors, 21 were followed up for a mean (median) period of 6.8±5.4 years (4.2 years). METHODS: We retrospectively reviewed 27 surgical embolectomy cases for massive or submassive acute PTE from 2003 to 2016. Immediate and long-term follow-up outcomes of surgical embolectomy were assessed on the basis of 30-day mortality, long-term mortality, postoperative complications, right ventricular systolic pressure, and tricuspid regurgitation grade. RESULTS: The 30-day and long-term mortality rates were 14.8% (4 of 27) and 4.3% (1 of 23), respectively. Three patients had major postoperative complications, including hypoxic brain damage, acute kidney injury, and endobronchial bleeding, respectively (3.7% each). Right ventricular systolic pressure (median [range], mm Hg) decreased from 62.0 (45.5–78.5) to 31.0 (25.7–37.0, p<0.001). The tricuspid valve regurgitation grade (median [range]) decreased from 1.5 (0.63–2.00) to 0.50 (0.50–1.00, p<0.05). The improvement lasted until the last echocardiographic follow-up. CONCLUSION: Surgical embolectomy revealed favorable mortality and morbidity rates in patients with acute massive or submassive PTE, with sustained long-term improvements in cardiac function.
Subject(s)
Humans , Acute Kidney Injury , Blood Pressure , Cardiopulmonary Bypass , Echocardiography , Embolectomy , Follow-Up Studies , Hemorrhage , Hypoxia, Brain , Mortality , Postoperative Complications , Pulmonary Embolism , Retrospective Studies , Survivors , Tricuspid Valve InsufficiencyABSTRACT
Upgaze or sustained elevation of the eyes, is an alteration of ocular motility initially described in hypoxic coma. We report a 65-year-old woman admitted with hypotension and alteration of sensorium due to the ingestion of 9.5 g of Bupropion. She presented two seizures of short duration, without epileptic activity on the EEG. She had a persistent asynchronous myoclonus in extremities, tachycardia and prolonged Q-t. She suffered a cardiac arrest caused by asystole, which recovered quickly in five minutes. At that moment, upgaze appeared, associated with a persistent ocular opening, which persisted for days, but finally disappeared, without remission of coma. A magnetic resonance imaging done at the eighth day, showed hyperintensity of the oval center and corpus callosum which disappeared in a new imaging study done 30 days later, where images of hypoxia in the basal nuclei and cortex appeared. The patient died forty seven days after admission. Up-gaze is an ominous oculomotor alteration linked to an important but incomplete damage in the cerebral cortex, a condition that perverts some sequences of the ocular opening, reversing the Bell phenomenon and producing eyelid retraction.
Subject(s)
Humans , Female , Aged , Ocular Motility Disorders/chemically induced , Hypoxia, Brain/chemically induced , Bupropion/adverse effects , Coma/chemically induced , Antidepressive Agents, Second-Generation/adverse effects , Drug Overdose/complications , Personality Disorders/drug therapy , Suicide , Magnetic Resonance Imaging , Fatal OutcomeABSTRACT
OBJECTIVE@#To investigate the effects of propofol combined with hypoxia on cognitive function of immature rats and the possible role of p38 pathway and tau protein in mediating such effects.@*METHODS@#Ninety 7-day-old (P7) SD rats were randomized for daily intraperitoneal injection of propofol (50 mg/kg) or lipid emulsion (5.0 mL/kg) for 7 consecutive days. After each injection, the rats were placed in a warm box (38 ℃) with an oxygen concentration of 18% (hypoxia), 21% (normal air), or 50% (oxygen) until full recovery of the righting reflex. Another 90 P7 rats were similarly grouped and received intraperitoneal injections of p-p38 blocker (15 mg/kg) 30 min before the same treaments. The phosphorylated tau protein, total tau protein and p-p38 content in the hippocampus were detected using Western blotting. The spatial learning and memory abilities of the rats were evaluated with Morris water maze test.@*RESULTS@#Compared with lipid emulsion, propofol injection resulted in significantly increased levels of p-p38, phosphorylated tau and total tau proteins in rats with subsequent hypoxic or normal air treatment ( < 0.05), but propofol with oxygen and injections of the blocker before propofol did not cause significant changes in the proteins. Without subsequent oxygenation, the rats receiving injections of propofol, with and without prior blocker injection, all showed significantly prolonged latency time and reduced platform-crossing times and third quadrant residence time compared with the corresponding lipid emulsion groups ( < 0.05). With oxygen treatment, the rats in propofoland blocker-treated groups showed no significant difference in the performance in Morris water maze test from the corresponding lipid emulsion group. The results of Morris water maze test differed significantly between blocker-propofol group and propofol groups irrespective of exposures to different oxygen levels ( < 0.05), but not between the lipid emulsion and blocker group pairs with exposures to different oxygen levels.@*CONCLUSIONS@#Propofol combined with hypoxia can affect the expression of tau protein through p38 pathway to impair the cognitive function of immature rats, in which oxygen plays a protective role.
Subject(s)
Animals , Rats , Cognitive Dysfunction , Metabolism , Hippocampus , Chemistry , Hypnotics and Sedatives , Pharmacology , Hypoxia, Brain , Metabolism , MAP Kinase Signaling System , Maze Learning , Physiology , Memory , Physiology , Propofol , Pharmacology , Random Allocation , Rats, Sprague-Dawley , tau ProteinsABSTRACT
Delayed anoxic encephalopathy after carbon monoxide (CO) poisoning is characterized by neurological deterioration that occurs after recovery from acute CO intoxication. There has been no established therapy. We report a patient recovered from acute CO intoxication developed various neurological symptoms. After the administration of high dose prednisolone and anticholinesterase inhibitor, the therapeutic effect was remarkable and confirmed by quantitative analysis of diffusion-tensor imaging (DTI). DTI could be used to evaluate the therapeutic effect for delayed anoxic encephalopathy after CO poisoning.
Subject(s)
Humans , Carbon Monoxide Poisoning , Carbon Monoxide , Carbon , Diffusion Tensor Imaging , Hypoxia, Brain , Leukoencephalopathies , Magnetic Resonance Imaging , Poisoning , PrednisoloneABSTRACT
This paper reports the effects of neuromuscular electrical stimulation (NMES) when applied to the facial muscles and submental region on a child with dysphagia. The subject was a 5 month girl who had hypoxic brain damage. Two electrodes were applied to the submental region horizontally (6.0 mA) and two electrodes were applied to each side of the mouth (5.0 mA). The child's jaw movement, swallowing food/liquid without excess loss, and swallowing without cough were improved. In addition, she could intake nutrition through the mouth. The result of the level on the Penetration Aspiration Scale (PAS) decreased from 4 to 1, the score on the Behavioral Assessment Scale of Oral Function in Feeding (BASOFF) increased from 13 to 17, and the level on the American Speech Language and Hearing Association: National outcomes measurements system (ASHA NOMS) increased from 1 to 3. When applying NMES to a child with dysphagia, the practitioner should consider various attachment places for improvements in the children's swallowing function.
Subject(s)
Child , Female , Humans , Hypoxia , Cough , Deglutition Disorders , Deglutition , Electric Stimulation , Electrodes , Facial Muscles , Hearing , Hypoxia, Brain , Jaw , MouthABSTRACT
PURPOSE: Quadriplegic children with cerebral palsy are more susceptible to osteoporosis because of various risk factors that interfere with bone metabolism. Pamidronate is effective for pediatric osteoporosis, but there are no guidelines for optimal dosage or duration of treatment in quadriplegic children with osteoporosis. We aimed to evaluate the efficacy of low-dose pamidronate treatment in these patients. METHODS: Ten quadriplegic patients on antiepileptic drugs (6 male, 4 female patients; mean age, 10.9±5.76 years), with osteoporosis and gross motor function classification system level V, were treated with pamidronate (0.5–1.0 mg/kg/day, 2 consecutive days) every 3–4 months in a single institution. The patients received oral supplements of calcium and vitamin D before and during treatment. The lumbar spine bone mineral density (BMD) z score and biochemical markers of bone metabolism were measured regularly during treatment. RESULTS: The main underlying disorder was perinatal hypoxic brain damage (40%, 4 of 10). The mean cumulative dose of pamidronate was 4.49±2.22 mg/kg/yr, and the mean treatment period was 10.8±3.32 months. The BMD z score of the lumbar spine showed a significant increase from −4.22±1.24 before treatment to −2.61±1.69 during treatment (P=0.008). Alkaline phosphatase decreased during treatmentn (P=0.037). Significant adverse drug reactions and new fractures were not reported. CONCLUSION: Low-dose pamidronate treatment for quadriplegic children with cerebral palsy increased lumbar BMD and reduced the incidence of fracture.
Subject(s)
Child , Female , Humans , Male , Alkaline Phosphatase , Anticonvulsants , Biomarkers , Bone Density , Calcium , Cerebral Palsy , Classification , Drug-Related Side Effects and Adverse Reactions , Hypoxia, Brain , Incidence , Metabolism , Osteoporosis , Quadriplegia , Risk Factors , Spine , Vitamin DABSTRACT
Carbon monoxide poisoning causes hypoxic brain damage with various neurological complications. Cerebral hemorrhagic infarction has rarely been reported as a complication of carbon monoxide poisoning. The author experienced a patient who developed cerebral infarction in the striatocapsular area extending to the corona radiata after carbon monoxide poisoning, which was followed by hemorrhagic transformation associated with neurological deterioration.
Subject(s)
Humans , Carbon Monoxide Poisoning , Carbon Monoxide , Carbon , Cerebral Infarction , Hemorrhage , Hypoxia, Brain , InfarctionABSTRACT
A 74-year-old man presented with recurrent vomiting and aspiration pneumonia in the left lower lobe. He entered the intensive care unit to manage the pneumonia and septic shock. Although a percutaneous endoscopic gastrostomy tube was implanted for recurrent vomiting, vomiting and aspiration recurred frequently during admission. Subsequently, he complained of neck pain when in an upright position. A videofluoroscopic swallowing study showed compression of the esophagus by cervical osteophytes and tracheal aspiration caused by an abnormality at the laryngeal inlet. Cervical spine X-rays and computed tomography showed anterior cervical osteophytes at the C3-6 levels. Surgical decompression was scheduled, but was cancelled due to his frailty. Unfortunately, further recurrent vomiting and aspiration resulted in respiratory arrest leading to hypoxic brain damage and death. Physicians should consider cervical spine disease, such as diffuse skeletal hyperostosis as an uncommon cause of recurrent aspiration pneumonia.
Subject(s)
Aged , Humans , Bays , Decompression, Surgical , Deglutition , Esophagus , Gastrostomy , Hyperostosis , Hypoxia, Brain , Intensive Care Units , Neck Pain , Osteophyte , Pneumonia , Pneumonia, Aspiration , Shock, Septic , Spine , VomitingABSTRACT
BACKGROUND/AIMS: Percutaneous endoscopic gastrostomy (PEG) is performed to provide enteral nutrition to patients who require tube-feeding support due to impaired oral intake. As life expectancy increases, the need for, and use of PEG also tend to increase. We aimed to evaluate the indications and complications of PEG insertion, and to investigate any differences in the complication group. MATERIALS AND METHODS: We conducted a retrospective analysis of 109 patients who received a PEG procedure between April 2011 and April 2016 in the Korea University Ansan Hospital. We reviewed the indications and complications related to PEG insertion and time interval of tube change. RESULTS: Among 109 patients who underwent a PEG procedure, 71.6% were male, and the mean age was 68.2 years. The most common indications for PEG were central nervous system diseases, including stroke (33.9%), cerebral hemorrhage (29.4%), and hypoxic brain damage (8.3%). The overall complication rate was 14.7%, and the most common complication was peristomal infection (7.3%). Most of the complications occurred within 10 days in 14 of 16 patients (87.5%). The patients with complications were older than those without complications (74.6±11.1 vs. 67.1±14.0 years, P=0.043). The mean time interval for gastrostomy tube change was 7.3 months. CONCLUSIONS: The most common indication of PEG was brain disease, and the complication rate cannot be ignored. Careful attention is needed after a PEG procedure especially in elderly patients.
Subject(s)
Aged , Humans , Male , Brain Diseases , Central Nervous System Diseases , Cerebral Hemorrhage , Endoscopy , Enteral Nutrition , Gastrostomy , Hypoxia, Brain , Korea , Life Expectancy , Retrospective Studies , StrokeABSTRACT
A 74-year-old man presented with recurrent vomiting and aspiration pneumonia in the left lower lobe. He entered the intensive care unit to manage the pneumonia and septic shock. Although a percutaneous endoscopic gastrostomy tube was implanted for recurrent vomiting, vomiting and aspiration recurred frequently during admission. Subsequently, he complained of neck pain when in an upright position. A videofluoroscopic swallowing study showed compression of the esophagus by cervical osteophytes and tracheal aspiration caused by an abnormality at the laryngeal inlet. Cervical spine X-rays and computed tomography showed anterior cervical osteophytes at the C3-6 levels. Surgical decompression was scheduled, but was cancelled due to his frailty. Unfortunately, further recurrent vomiting and aspiration resulted in respiratory arrest leading to hypoxic brain damage and death. Physicians should consider cervical spine disease, such as diffuse skeletal hyperostosis as an uncommon cause of recurrent aspiration pneumonia.
Subject(s)
Aged , Humans , Bays , Decompression, Surgical , Deglutition , Esophagus , Gastrostomy , Hyperostosis , Hypoxia, Brain , Intensive Care Units , Neck Pain , Osteophyte , Pneumonia , Pneumonia, Aspiration , Shock, Septic , Spine , VomitingABSTRACT
Abstract Background and objectives: Isoflurane is halogenated volatile ether used for inhalational anesthesia. It is widely used in clinics as an inhalational anesthetic. Neonatal hypoxic ischemia injury ensues in the immature brain that results in delayed cell death via excitotoxicity and oxidative stress. Isoflurane has shown neuroprotective properties that make a beneficial basis of using isoflurane in both cell culture and animal models, including various models of brain injury. We aimed to determine the neuroprotective effect of isoflurane on hypoxic brain injury and elucidated the underlying mechanism. Methods: A hippocampal slice, in artificial cerebrospinal fluid with glucose and oxygen deprivation, was used as an in vitro model for brain hypoxia. The orthodromic population spike and hypoxic injury potential were recorded in the CA1 and CA3 regions. Amino acid neurotransmitters concentration in perfusion solution of hippocampal slices was measured. Results: Isoflurane treatment caused delayed elimination of population spike and improved the recovery of population spike; decreased frequency of hypoxic injury potential, postponed the onset of hypoxic injury potential and increased the duration of hypoxic injury potential. Isoflurane treatment also decreased the hypoxia-induced release of amino acid neurotransmitters such as aspartate, glutamate and glycine induced by hypoxia, but the levels of γ-aminobutyric acid were elevated. Morphological studies showed that isoflurane treatment attenuated edema of pyramid neurons in the CA1 region. It also reduced apoptosis as evident by lowered expression of caspase-3 and PARP genes. Conclusions: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.
Resumo Justificativa e objetivos: Isoflurano é um éter volátil halogenado usado para anestesia por via inalatória. É amplamente usado na clínica como um anestésico para inalação. A lesão hipóxico-isquêmica neonatal ocorre no cérebro imaturo e resulta em morte celular tardia via excitotoxicidade e estresse oxidativo. Isoflurano mostrou ter propriedades neuroprotetoras que formam uma base benéfica para o seu uso tanto em cultura de células quanto em modelos animais, incluindo vários modelos de lesão cerebral. Nosso objetivo foi determinar o efeito neuroprotetor de isoflurano em hipóxia cerebral e elucidar o mecanismo subjacente. Métodos: Fatias de hipocampo, em fluido cerebrospinal artificial (CSFA) com glicose e privação de oxigênio, foram usadas como um modelo in vitro de hipóxia cerebral. O pico de população ortodrômica (PPO) e o potencial de lesão hipóxica (PLH) foram registrados nas regiões CA1 e CA3. A concentração de neurotransmissores de aminoácidos na solução de perfusão das fatias de hipocampo foi medida. Resultados: O tratamento com isoflurano retardou a eliminação do PPO e melhorou a recuperação do PPO; diminuiu a frequência do PLH, retardou o início do PLH e aumentou a duração do PLH. O tratamento com isoflurano também diminuiu a liberação de neurotransmissores de aminoácidos induzida pela hipóxia, como aspartato, glutamato e glicina, mas os níveis de ácido γ-aminobutírico (GABA) estavam elevados. Estudos morfológicos mostram que o tratamento de edema com isoflurano atenuou o edema de neurônios piramidais na região CA1. Também reduziu a apoptose, como mostrado pela expressão reduzida da caspase-3 e genes PARP. Conclusões: Isoflurano mostrou um efeito neuroprotetor na lesão neuronal no hipocampo induzida por hipóxia através da supressão de apoptose.