Relevant bibliographies by topics / Encephalopaty

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Encephalopaty'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Encephalopaty"

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Tonello, S., S. Montagnese, S. Schiff, P. Amodio, P. Bizzotto, P. Pesce, A. Gatta, M. Bolognesi, D. Sacerdoti, and G. Bombonato. "245 SPLENO-SYSTEMIC SHUNTS AND COVERT HEPATIC ENCEPHALOPATY." Journal of Hepatology 58 (April 2013): S105. http://dx.doi.org/10.1016/s0168-8278(13)60247-0.

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Sturniolo, L., F. Balzola, A. Ottobrelli, M. Torrani, S. Martini, E. Morello, A. Smedile, et al. "229 GLUTEN/CASEIN-FREE DIET AND LIVER ENCEPHALOPATY." Journal of Hepatology 50 (April 2009): S93. http://dx.doi.org/10.1016/s0168-8278(09)60231-2.

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Rakhimbaeva, G. S. "242 Methabolic encephalopaty: basis factors in apoptotic cells." International Journal of Developmental Neuroscience 14 (July 1996): 109. http://dx.doi.org/10.1016/0736-5748(96)80431-x.

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Sorodoc, Laurentiu, Catalina Lionte, Victorita Sorodoc, Ovidiu Petris, and Irina Jaba. "Is MARS system enough for A.phalloides-induced liver failure treatment?" Human & Experimental Toxicology 29, no. 10 (February 23, 2010): 823–32. http://dx.doi.org/10.1177/0960327110363327.

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Patients with Amanita phalloides-induced liver failure (LF) have a high mortality, despite significant advances in intensive care managemet. Our study evaluated the effect of Molecular Absorbents Recirculating System (MARS) comparative with optimal intensive care (OIC) in adults with this condition, in the absence of liver transplantation (LT). Six consecutive patients (women, range 16—61 years) affected by A.phalloides-induced LF were treated with OIC (3 patients) and MARS (3 patients). Laboratory parameters and hepeatic encephalopaty were evaluated 15 min before and 24 hours following each MARS treatment. Three 6-hour sessions per patient were performed in MARS group, with a statistically significant decrease in ammonia (p value 0.011), alaninaminotransferase (ALT) and prothrombin time (PT) (p value 0.004). Two patients had a significant rebound in bilirubin (+116%; p value 0. 04) 24 hours following MARS. Mortality in MARS group was 66.7%. Survival rate in OIC was 0%. Negative prognostic markers: lack of PT and hepatic encephalopaty improvement, rebound in bilirubin, and delay of MARS therapy initiation. No significant adverse reactions occurred during MARS. MARS is an effective depurative therapy in adults with A.phalloides-induced LF, but alone is not enough. Survival is predicted by the results of the initial MARS, amount of mushroom consumed, and time from toxin exposure.
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Puryatni, Anik, and Tom J. de Koning. "ENCEPHALOPATY AKUT PADA ANAK DENGAN KELAINAN METABOLISME BAWAAN (PENDEKATAN PRAKTIS)." Jurnal Kedokteran Brawijaya 24, no. 3 (March 19, 2008): 3–2008. http://dx.doi.org/10.21776/ub.jkb.2008.024.03.7.

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Soto, S., E. Castro, J. L. Ulla, S. Vazquez, R. Baltar, V. Alvarez, J. Vazquez-Sanluis, L. Ledo, and E. Vazquez-Astray. "313 HYDROXIZYNE IMPROVED INSOMNIA IN CIRRHOTIC INPATIENTS WITH GRADE I ENCEPHALOPATY." Journal of Hepatology 48 (January 2008): S124. http://dx.doi.org/10.1016/s0168-8278(08)60315-3.

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ARMENDARIZBORUNDA, J., J. GALVEZGASTELUM, A. SEGURAFLORES, C. BEASZARATE, and A. MIRANDA. "366 Combined hupa plus MMP-8 gene therapy reverts cirrhosis and improves hepatic encephalopaty." Hepatology 38 (2003): 336–37. http://dx.doi.org/10.1016/s0270-9139(03)80409-3.

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Pironti, Erica, Francesca Cucinotta, Francesca Granata, Maria Spanò, Maria Bonsignore, Henry Houlden, Vincenzo D. Salpietro, Antonella Gagliano, and Gabriella Di Rosa. "Preliminary Results of Whole Exome Sequencing in a Cohort of Sicilian Children with Early-Onset Epileptic Encephalopaty." European Journal of Paediatric Neurology 21 (June 2017): e169. http://dx.doi.org/10.1016/j.ejpn.2017.04.718.

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Bombushkar, Igor, Anatoliy Gozhenko, Mykhaylo Korda, Xawery Żukow, and Igor Popovych. "Peculiarities of relationships between plasma levels of nitrogenous metabolites and EEG & HRV parameters in patients with postradiation encephalopaty." Journal of Education, Health and Sport 12, no. 10 (October 31, 2022): 335–55. http://dx.doi.org/10.12775/jehs.2022.12.10.040.

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Background. Recently we shown that nitrogenous plasma metabolites (uric acid, bilirubin, urea and creatinine), even in the absence of uremia, are able to influence the state of the anxiety, autonomic and central nervous and endocrine systems, apparently through aryl hydrocarbon and adenosine receptors of neurons and endocrine cells and/or directly. Sexual dimorphism in the neurotropic effects of uric acid in neurologically healthy patients was also revealed. The purpose of this study is to compare nitrogenous-neural relationships in neurologically healthy men and those with post-radiation encephalopathy (PREP). Materials and Methods. The object of observation were neurologically healthy 31 men (24÷69 y) and 19 patients (26÷61 y) with PREP. The relationships between plasma levels of nitrogenous metabolites, on the one hand, and EEG and HRV parameters, on the other, were analyzed. Results. By constructing regression models with stepwise elimination it was found that the multiple correlation coefficient (R±µ) of creatinine with neural parameters in patients with PREP significantly exceeded that of control patients (0,762±0,069 vs 0,409±0,107; t=2,62; p=0,011). With regard to urea, the differences are insignificant (0,801±0,059 vs 0,694±0,066; t=1,17; p>0,2), and with regard to bilirubin (0,548±0,115 vs 0,402±0,107; t=0,94) and uric acid (0,496±0,124 vs 0,549±0,089; t=0,32), there are practically no differences. Conclusion. Post-radiation encephalopathy is accompanied not only by deviations from the norm of a number of EEG and HRV parameters, but also by their increased sensitivity to creatinine and, to a lesser extent, urea, but not to bilirubin and uric acid.
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Yulianti Bisri, Dewi, and Tatang Bisri. "Pertimbangan Anestesi Perioperatif untuk Pasien Bedah Saraf dengan Covid-19." Jurnal Neuroanestesi Indonesia 10, no. 1 (February 19, 2021): 55–62. http://dx.doi.org/10.24244/jni.v10i1.324.

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The novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, Hubei province China, in December 2019, and spread fast to all the world more than 190 countries. Patients should be screened for covid-19 using a combination of history, computed tomography (CT) chest, and real time quantitative polymerase chain reaction (RT-qPCR) testing depending on institutional policies. Neurological symptom as dizziness, headache, hypogeusia and hyposmia, common (36%) at covid-19 patient. Encephalopaty and changed mental status exist in patient infected by SARS-CoV-2 virus. Cerebrovascular diseases more in severe covid-19; acute ischemic stroke had reported in 5.7% and altered level of consciousnes in 15% patient. Surgical measuremet cranial and spinal rutine is safe, endoscopic endonasal surgery not safe and must be avoided. Extubation after general anesthesia if possible do air negative pressure room, and personil still use personal protection equipment (PPE) level 3. Must be avoid patient cough during extubation. After extubation, give oxygen nasal canule, surgical mask, and high flow oxygen (give <6 L/min) avoided given the risk of aerosolization
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Dissertations / Theses on the topic "Encephalopaty"

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MURANO, CARMEN. "Channelopathies and epileptic syndromes: characterization of novel variants associated with progressive epileptic encephalopathy and in vitro validation of therapeutic approaches." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/365090.

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L’epilessia è un disturbo neurologico caratterizzato da episodi ricorrenti di disfunzioni elettriche cerebrali chiamate crisi epilettiche. Il coinvolgimento dei canali ionici HCN (Hyperpolarization-activated Cyclic Nucleotide-gated) nel processo di epilettogenesi è stato recentemente messo in evidenza. Questo studio presenta il caso di un paziente affetto da encefalopatia epilettica progressiva farmaco-resistente. La malattia è caratterizzata da un grave ritardo nello sviluppo, atassia, distonia, deficit visivo cerebrale. L’analisi genetica ha riscontrato nel paziente una mutazione missenso a carico del gene HCN2 cha causa una sostituzione amminoacidica a livello del residuo Glicina in posizione 460 del segmento transmembrana S6 (p.Gly460Asp). Esperimenti condotti con la tecnica del patch-clamp in modalità whole-cell su cellule HEK293 e su colture primarie di neuroni corticali di ratti neonatali hanno evidenziato una significativa riduzione della corrente ionica in presenza della mutazione. Inoltre, risulta alterata anche l’eccitabilità della membrana neuronale. Gli esperimenti di immunofluorescenza suggeriscono una compromissione della traslocazione della proteina HCN2 mutata in membrana, la quale sembra accumularsi in posizione peri-nucleare. Inoltre, la proteina mutata p.Gly460Asp ha effetti negativi anche sulla funzionalità del canale HCN1, con il quale HCN2 forma eteromeri funzionali. Si tratta quindi di una mutazione che provoca una loss-of-function della proteina coinvolta e che, potenzialmente, ha effetto anche sul controllo generale dell’eccitabilità neuronale. I dati ottenuti sono parte di un manoscritto che verrà a breve sottomesso. Dal punto di vista farmacologico, il paziente mostra un’eccellente risposta clinica alla dieta chetogenica, un regime alimentare ad alto contenuto di grassi e bassa quantità di carboidrati che, attraverso la β-ossidazione degli acidi grassi, porta alla produzione epatica di corpi chetonici, usati in molti tessuti extra-epatici come fonte di energia e come agenti pleiotropici ad azione anti-infiammatoria. Pertanto, si ritiene che il regime chetogenico possa migliorare le condizioni cliniche dei pazienti influenzando l’organismo nel suo insieme. Per queste ragioni, una linea della ricerca condotta si è concentrata sugli effetti di ambiente chetogenico su una coltura neuronale. L’interesse riguardo gli effetti positivi della dieta chetogenica su pazienti epilettici, ha portato alla pubblicazione di una review (Murano C, et al. Effect of the ketogenic diet in excitable tissues. Am J Physiol Cell Physiol. 2021;320(4):C547-C553. doi: 10.1152/ajpcell.00458.2020. PMID: 33502948), mentre per quanto riguarda la sezione sperimentale, i dati sono parte di un manoscritto attualmente in preparazione. L’encefalopatia epilettica dello sviluppo è associata anche a varianti in canali di potassio voltaggio dipendenti della sottofamiglia Q membro 2 (KCNQ2). Grazie ad una collaborazione in essere con l’Università Federico II di Napoli, la variante p.G310S nel gene KCNQ2, responsabile del disturbo, è stata caratterizzata in un modello di cellule CHO (Chinese Hamster Ovary) e in un modello di neuroni corticali derivanti da ratti neonatali risultando in una loss-of-function. Il paziente portatore della mutazione mostrava una completa disorganizzazione dell’attività di fondo nelle registrazioni elettroencefalografiche (EEG), migliorate dopo trattamento con Gabapentin, un attivatore del canale. Sono stati indagati gli effetti di Gabapentin su questa specifica mutazione p.G310S fornendo prove dell’effetto positivo nel trattamento dell’encefalopatia epilettica dello sviluppo causata da mutazioni loss-of-function a carico di KCNQ2. I risultati ottenuti sono stati recentemente pubblicati (Soldovieri MV, et al. Gabapentin treatment in a patient with KCNQ2 developmental epileptic encephalopathy. Pharmacol Res. 2020;160:105200. doi: 10.1016/j.phrs.2020.105200. PMID: 32942014).
Epilepsy is a chronic neurological disorder supported by recurrent episodes of brain electrical dysfunctions called epileptic seizures. The involvement of HCN (Hyperpolarization-activated Cyclic Nucleotide-gated) ion channels in the epileptogenesis process has recently been highlighted. This study presents the case of a patient with drug-resistant progressive epileptic encephalopathy. Clinically, the disease is characterized by severe developmental delay, ataxia, dystonia, cerebral visual impairment. Genetic analysis revealed the presence in the DNA of the patient a missense mutation in the HCN2 gene which causes an amino acid substitution at the level of the Glycine residue in position 460 of the transmembrane segment S6 (p.Gly460Asp). Experiments conducted with the whole-cell patch-clamp technique on HEK293 cells and primary cultures of cortical neurons from neonatal rats showed a significant reduction in the ion current density when the mutation was present. Furthermore, the excitability of the neuronal membrane was also altered. Immunofluorescence experiments suggest an impairment of the translocation of the membrane-mutated HCN2 protein, which appears to accumulate in a peri-nuclear position. Furthermore, the mutated protein p.Gly460Asp also had negative effects on the functionality of the HCN1 channel, with which HCN2 forms functional heteromers. Therefore, this mutation causes a loss-of-function of the protein involved and, potentially, it also has an effect on the general control of neuronal excitability. The data obtained are part of a manuscript that will be submitted shortly. The patient showed an excellent clinical response to the ketogenic diet, a high fat and low carbohydrates diet which, through the β-oxidation of fatty acids, leads to the hepatic production of ketone bodies, used in many extra-hepatic tissues as a source of energy and as pleiotropic and anti-inflammatory agents. Ketogenic regimen can improve the clinical condition of patients affect the organism as a whole. For these reasons, a line of research conducted has focused on the effects of the ketogenic environment on a neuronal culture and in particular on the characterization of the p.Gly460Asp mutation. The interest in the positive effects of the ketogenic diet on epileptic patients led to the publication of a review (Murano C, et al. Effect of the ketogenic diet in excitable tissues. Am J Physiol Cell Physiol. 2021; 320 (4): C547-C553. Doi: 10.1152 / ajpcell.00458.2020. PMID: 33502948), while for the experimental section, the data are part of a manuscript currently in preparation. Developmental epileptic encephalopathy is also associated with variants in voltage-dependent potassium channels of the subfamily Q member 2 (KCNQ2). Thanks to an existing collaboration with Prof. Taglialatela at the Federico II University of Naples, the p.G310S variant in the KCNQ2 gene, responsible for early onset epileptic encephalopathy, has been functionally characterized in a CHO (Chinese Hamster Ovary) cell model and in a model of cortical neurons derived from neonatal rats resulting in a loss-of-function. The patient carrying the mutation showed a complete disorganization of the background activity in the electroencephalographic (EEG) recordings. The "burst-suppression pattern" shown in the EEG improved after treatment with Gabapentin, a channel activator. Based on this clinical improvement, the effects of Gabapentin on p.G310S mutation were investigated providing evidence of the positive effect of this specific drug in the treatment of developmental epileptic encephalopathy caused by loss-of-function mutations by KCNQ2. Again, the results obtained have been recently published (Soldovieri MV, et al. Gabapentin treatment in a patient with KCNQ2 developmental epileptic encephalopathy. Pharmacol Res. 2020; 160: 105200. Doi: 10.1016 / j.phrs.2020.105200. PMID : 32942014).
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Wadzinski, Jim, Ronald Franks, David S. Roane, and Max Bayard. "Valproate Associated Hyperammonemic Encephalopathy." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/7167.

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The use of valproic acid (VPA) (also known as Depakote, Depakene, and others) frequently results in elevated plasma ammonia. In some people, hyperammonemia may be clinically significant, resulting in hyperammonemic encephalopathy, which may be severe. Valproic acid-induced hyperammonemic encephalopathy may occur in people with normal liver function, despite normal doses and serum levels of VPA. We describe 2 cases of valproic acid-induced hyperammonemic encephalopathy in patients with supratherapeutic VPA levels, although the condition has been described in people with normal VPA levels. With the increasing indications and off-label uses of VPA, family physicians should be aware of this potential complication of VPA and check ammonia levels in patients taking VPA who present with alterations in mental status. Treatment with L-carnitine may be beneficial in reducing ammonia levels. Valproic acid (VPA) is effective in the treatment of seizure disorders, bipolar disorder, migraine headache prophylaxis, neuropathic pain, restless legs syndrome, dementia-related agitation, and social anxiety disorder, among other conditions. VPA has numerous drug interactions and toxicities; severe toxicities include hepatic damage, pancreatitis, teratogenicity, thrombocytopenia, and hyperammonemia. Here we depict 2 case reports of VPA-induced hyperammonemic encephalopathy (VHE), both occurring in patietns with no history of underlying liver disease. In one instance, the patient was able to function, but with significant cognitive limitations. In the second case, the patient was comatose. Both of the patients we describe also had supratherapeutic VPA levels, but VHE is a well-documented potential complication of the use of VPA in the medical literature, and it may occur in people with normal VPA levels.1 Because of the wide spectrum of symptoms associated with VHE, physicians should consider hyperammonemia in the differential diagnosis of any patient taking VPA who shows changes in behavior, cognition, or orientation
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Hadjihambi, Anna. "Neurochemistry of the hepatic encephalopathy." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10038691/.

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The pathogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactorial and the role of ammonia remains controversial. Experimental studies conducted in animal (rat) models of HE, in combination with pharmacological approaches, were used to test the hypothesis that during HE, chronic exposure to elevated ammonia concentrations alters cerebral oxygenation, compromises lactate transport between astrocytes and neurons, and impairs uptake of neurotransmitters. It was also hypothesised that HE impairs glymphatic clearance mechanisms, either as a cause or a consequence of the disease, which exacerbates the detrimental central nervous effects of the accumulated toxins. The results of the experiments described in this thesis suggest that in HE: a) ammonia compromises cerebral oxygenation, but does not affect cerebrovascular reactivity, b) ammonia mediates cortical hemichannel dysfunction and impairs channel-mediated lactate release, potentially interfering with the astrocyte-neuron lactate shuttle, c) hyperammonemia results in a significant increase in cortical extracellular glutamate concentration, which is exacerbated under hypoxic conditions, and d) efficacy of glymphatic clearance is affected in discrete regions of the brain, which aligns with specific cognitive/behavioral impairments. These findings provide the first evidence of a critical pathophysiological role of ammonia in inducing neuronal energy deficit in HE due to impaired cerebral oxygenation, compromised hemichannel-mediated lactate transport between astrocytes and neurons and affected glymphatic clearance.
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Tvayedg, Naceem Saad Munan. "Attention function in children undergoing encephalopathy." Thesis, Sumy State University, 2015. http://essuir.sumdu.edu.ua/handle/123456789/41252.

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Gorden, Zachary Newton. "Chronic traumatic encephalopathy: a literary review." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12398.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
As early as the 1920's it has been established that repetitive brain trauma, through activities such as boxing, can lead to progressive neurological degeneration. This was termed Dementia Pugilistica until the more recent and greater encompassing term Chronic Traumatic Encephalopathy came into use. Chronic Traumatic Encephalopathy is a progressive neurodegenerative disease that is believed to be caused, or at least associated with, repetitive brain trauma on the concussive and sub concussive level. Clinically, Chronic Traumatic Encephalopathy is associated with a bevy of abnormal symptoms; ranging from personality changes, behavioral abnormalities, memory and mood disturbances as well as certain Parkinsonian symptoms like speech and gait abnormalities. Pathologically, Chronic Traumatic Encephalopathy is distinguished by a certain gross scale criteria, including but not limited too: wide spread atrophy of the brain tissue (most notably the cerebral hemispheres) and dilation of the ventricles and fenestration of the cavum septum pellucidum. The microscopic pathology of Chronic Traumatic Encephalopathy is also well established; it consists of extensive tau-immunoreactive neurofibrillary tangles and neuropil neurites concentrated in the depths of the sulci and perivascularly. In roughly half the cases of Chronic Traumatic Encephalopathy there is deposition of beta-amyloid plaques along with the tau-immunoreactive neurofibrillary tangles. Chronic Traumatic Encephalopathy can only be diagnosed post-mortem, leading to a vast array of issues in the detection and treatment of the disease. Much research has gone into potential diagnostic techniques that could greatly alter the lives of the athletes, military and civilians who are su±Iering from the symptoms of this disease. There is strong belief that early detection methods will be found, and these ideas center around in vivo imaging techniques, such as; Functional Magnetic Resonance Imaging and Single Photon Emission Computed Tomography, that would allow for physicians to pathologies before their overwhelming detriment. There is also study into proposed biomarkers, such as apolipoprotein-E, that could give indication of a higher susceptibility to degenerative neurologic disease such as Chronic Traumatic Encephalopathy.
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DI, MEO IVANO. "Altered Sulfide Metabolism in Ethylmalonic Encephalopathy." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29887.

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Ethylmalonic Encephalopathy, EE, is an autosomal recessive, invariably fatal disorder characterized by early-onset brain failure, microangiopathy, chronic diarrhoea, defective cytochrome c oxidase (COX) in muscle and brain, and high excretion of ethylmalonic acid (EMA) in urine. ETHE1, a gene encoding a mitochondrial beta-lactamase-like, iron-coordinating metalloprotein, is mutated in EE. We generated an Ethe1-null mouse that manifested the EE cardinal features. We found that thiosulfate was excreted in massive amount in urines of both Ethe1-/- mice and EE patients. High thiosulfate (H2SSO3) and sulfide (H2S) levels were present in Ethe1-/- mouse tissues. Sulfide is a powerful inhibitor of COX and terminal beta-oxidation, with vasoactive and vasotoxic effects that could explain the microangiopathy in EE patients. Sulfide is detoxified by a mitochondrial pathway that includes a sulfur dioxygenase (SDO). SDO activity was absent in Ethe1-/- mice, whereas ETHE1 overexpression in HeLa cells and E. coli markedly increased it. Therefore, ETHE1 is a mitochondrial SDO involved in catabolism of sulfide, which accumulates to toxic levels in EE. An important question that warranted the PhD experimental work concerns the source of H2S in ETHE1 mutant patients, and how accumulated sulfide can act on the cytochrome c oxidase complex at molecular level. The presence of elevated levels of thiosulfate in several tissues of the Ethe1-/- mouse suggests endogenous production of H2S from catabolism of cysteine and other sulfur-containing organic compounds. H2S is also a major product of the intestinal bacterial flora, especially anaerobic species residing in the colon. The presence of a gradient of COX deficiency in luminal vs. cryptal colonocytes in Ethe1-/- colon mucosa suggests that a defect of ETHE1-SDO activity results in faulty detoxification of exogenously produced H2S. In order to achieve effective reduction of H2S production, it is crucial to clarify which are the sources of this compound in the body that can then constitute specific targets for therapy. Another important issue is to understand the organ-specific mechanisms, which lead to failure of some organs, such as the brain and the skeletal muscle, but not of others, such as the liver. These aims can be implemented through the creation and characterization of conditional tissue-specific KO animals. A further research line concerns the improvement of biochemical and molecular approaches for the diagnosis of EE.
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Vessal, Mani. "A spongiform encephalopathy outbreak, anthropophagy or not?" Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ48417.pdf.

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Shawcross, Deborah Lindsay. "Ammonia, infection and inflammation in hepatic encephalopathy." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445060/.

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For over a century, we have known that ammonia is important in the pathogenesis of hepatic encephalopathy. Studies in patients with acute liver failure have shown rapid progression to severe encephalopathy in those patients with evidence of a systemic inflammatory response, suggesting a possible link between inflammation and encephalopathy. In view of the growing evidence to support the role of inflammation in increasing the susceptibility of the brain to the effects of hyperammonemia in liver disease, 3 hypotheses were explored: 1: Inflammation and infection are important in hepatic encephalopathy. 2: Inflammation and infection act synergistically with ammonia. 3: Ammonia makes the immune system more susceptible to infection. In the first of 2 clinical studies, inflammation was shown to be an important determinant of the presence and severity of minimal hepatic encephalopathy. In a second study, significant deterioration of neuropsychological test scores in patients with cirrhosis following induced hyperammonemia during the inflammatory state, but not after its resolution, suggested that inflammation may be important in modulating the cerebral effect of ammonia in liver disease, supporting the first hypothesis. Ammonia and inflammation were shown to be synergistic in the bile duct ligated rat which showed increased brain water and astrocyte swelling exacerbated by endotoxin and accompanied by a rise in nitric oxide and brain nitrotyrosine, but not in plasma ammonia, suggesting nitric oxide may play an important synergistic role in the pathogenesis of hepatic encephalopathy. Ammonia was shown to impair neutrophil function by reducing phagocytosis, inducing spontaneous respiratory burst and cell swelling. The p38"MAPK pathway was shown to be important and a p38"MAPK agonist prevented neutrophils from swelling in the presence of ammonia and improved phagocytosis. While cultures of muscle cells were a potentially interesting direction to take to investigate the effect of inflammation on the muscle uptake of ammonia, unfortunately the resulting data demonstrated a low glutamine synthetase activity. In conclusion, these studies illustrate the important factors that modulate the manifestation of symptoms of hepatic encephalopathy in cirrhosis, the most important of which is the synergistic role of inflammation and ammonia. Furthermore, the ammonia-induced impairment of neutrophil function may, in part, account for the increased susceptibility to infection found in patients with cirrhosis.
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Vessal, Mani Carleton University Dissertation Sociology and Anthropology. "A Spongiform encephalopathy outbreak: anthropophagy or not?" Ottawa, 1999.

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Bergqvist, Peter B. F. "Tryptophan-related neurotransmission in the brain disturbances associated with experimental hepatic encephalopathy /." Lund : Dept. of Clinical Pharmacology, Institute of Labortaory Medicine, Lund University Hospital, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39761954.html.

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Books on the topic "Encephalopaty"

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Food and Agriculture Organization of the United Nations. Regional Office for Latin America and the Caribbean. and Asociación Panamericana de Ciencias Veterinarias., eds. Novedades sobre la encefalopatia espongiforme de los bovinos =: News on the bovine spongiform encephalopaty. Santiago, Chile: Oficina Regional de la FAO para América Latina y el Caribe, 1996.

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Mullen, Kevin D., and Ravi K. Prakash, eds. Hepatic Encephalopathy. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-836-8.

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McCandless, David W., ed. Metabolic Encephalopathy. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-79112-8.

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Butterworth, Roger F., and Gilles Pomier Layrargues, eds. Hepatic Encephalopathy. Totowa, NJ: Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4506-3.

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1941-, McCandless David W., ed. Metabolic encephalopathy. New York: Springer, 2009.

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Hepatic encephalopathy. Boston: Butterworth-Heinemann, 1992.

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Gibbs, Clarence J., ed. Bovine Spongiform Encephalopathy. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4612-2406-8.

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Swanson, Janice C. Bovine spongiform encephalopathy. Beltsville, Md: National Agricultural Library, 1990.

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Pratt, Kendra. Bovine spongiform encephalopathy. Riverdale, MD: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, 1995.

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United States. Animal and Plant Health Inspection Service. Veterinary Services. Bovine spongiform encephalopathy. Hyattsville, Md.?]: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, 1994.

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Book chapters on the topic "Encephalopaty"

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Poretti, Andrea, and Thierry A. G. M. Huisman. "Encephalopathy." In Neonatal Head and Spine Ultrasonography, 51–74. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-14568-6_5.

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Larson, Jennifer C. G., and Yana Suchy. "Encephalopathy." In Encyclopedia of Clinical Neuropsychology, 1302. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_524.

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Larson, Jennifer C. G., and Yana Suchy. "Encephalopathy." In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_524-3.

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Serrano-Pozo, Alberto. "Encephalopathy." In The Wiley Handbook on the Aging Mind and Brain, 553–90. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781118772034.ch25.

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Wright, Wendy L. "Encephalopathy." In Handbook of Neurocritical Care, 19–30. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-772-7_2.

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Cooley, Laura A., Daniel G. Bausch, Marija Stojkovic, Waldemar Hosch, Thomas Junghanss, Marija Stojkovic, Waldemar Hosch, et al. "Encephalopathy." In Encyclopedia of Intensive Care Medicine, 845. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1534.

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Sataloff, Johnathan, and Robert T. Sataloff. "Encephalopathy." In Encyclopedia of Otolaryngology, Head and Neck Surgery, 762. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-23499-6_200190.

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Lewis, Steven L. "Encephalopathy." In Emergency Neurology, 283–94. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-0-387-88585-8_15.

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Lewis, Steven L. "Encephalopathy." In Emergency Neurology, 305–16. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75778-6_15.

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Imam, Ibrahim. "Encephalopathy." In 700 Essential Neurology Checklists, 17–21. New York: CRC Press, 2021. http://dx.doi.org/10.1201/9781003221258-8.

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Conference papers on the topic "Encephalopaty"

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Faur, Maria Eduarda, Emily Stefhani Keil, Gabriel Augusto Corti, Maria Eduarda Angelo de Mendonça Filet, Raddib Eduardo Noleto da Nóbrega de Oliveira, Rafael Pereira Guimarães, Thábata Emanuelle Martins Nunes, Gustavo da Cunha Ribas, Carla Heloísa Cabral Moro, and Alexandre Luiz Longo. "Creutzfeldt-Jakob disease: case report strongly suspicious with 14- 3-3 protein missing." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.059.

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Context: The Creutzfeldt-Jakob disease (CJd) is a rare spongiform encephalopathy caused by a prion. In clinical practice the presence of 14- 3-3 protein can be a insensitive marker of sporadic CJd, well as absent for genetic CJd and new variantes, being susceptible to false negatives. Case report: V.L, male, 57 years old, previously rigid, who presented na insidious picture of memory loss and a progressive functional decline for one month and a half. On admission, he was alert, non-contacting, with evidente myoclonus in the upper and lower members and spasticity in lower members. The picture is compatible with rapidly progressive dementia, and the hypothesis of CJd was suggested. The skull CT showed microangiopathy. Clean looking CSF, negative bacteroscopy, non-reactive VDRL, negative nanquim exam and missing 14-3-3 protein search. EEG recorded abnormal rhythm secondary to moderate diffuse and persistente encouragement of fund activity, indicating mild diffuse brain dysfunction, possibly encephalopatic. Skull MRI, signs of restriction and diffusion compromising the caudate nucleus of the putamen bilaterally and symmetrically, and the parietal córtex, predominantly the left, compatible with CJd. Patient had normal thyroid function and hypovitaminosis of mild B12, corrected with intramuscular injection. Evolved in 25 days to akinetic mutism and died in one month due to bronchial aspiration pneumonia. Conclusions: The CJd is a pathology difficult to diagnose, the 14-3-3 protein research is subject to bias, the clinical and radiological findings strongly indicate CJd.
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Herzberg, Emily M., Jessica Landers, Kimberly F. Greco, Henry A. Feldman, Arnold J. Sansevere, and Janet S. Soul. "Improving the Diagnosis of Neonatal Encephalopathy: Validation of a Novel Encephalopathy Scale for Hypoxic-Ischemic Encephalopathy (HIE) using Electroencephalogram (EEG)." In AAP National Conference & Exhibition Meeting Abstracts. American Academy of Pediatrics, 2021. http://dx.doi.org/10.1542/peds.147.3_meetingabstract.711.

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Pimenta, Marina Luiza, Jessica Andrade de Oliveira, Herval Ribeiro Soares Neto, Sonia Maria Cesar de Azevedo Silva, and Luiza Ferrari de Castro Melo. "Atypical presentation of tacrolimus encephalopathy in a kidney transplant patient." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.452.

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Context: Neurological complications triggered by tacrolimus in transplant patients can occur in a common way. Tacrolimus encephalopathy is a rare presentation. The present case follows atypical patterns of this disease, since it presented as aphasia, seizure and unusual radiological findings. Case report: A 52--year--old female patient complaining of severe headache for 3 days, associated with difficulty in formulating phrases and confusion. She had a history of nephrolithiasis, kidney transplantation (2020), hypertension and diabetes, using tacrolimus, mycophenolate and prednisone. In the hospital, she had a global aphasia and episodes of generalized tonic-- clonic seizures, being medicated with levetiracetam, phenytoin and acyclovir, maintaining good seizure control, but persisting aphasic. Brain MRI showed an extensive hypersignal in T2/FLAIR involving the left parieto-- occipito-- temporal cortical subcortical region. CSF showed: protein 91 mg/dL, glucose 143 mg/dL and leukocytes 2 cells/mm³. Negative infectious screening was performed in the CSF using FilmArray encephalitis/meningitis panel. Hypothesized an encephalopathy caused by tacrolimus we discontinued the medication and after 3 days, the patient had a significant clinical improvement, no aphasia and drastic reduction in the hypersignal extension. The patient was discharged from service using cyclosporine and prednisone. Conclusions: Tacrolimus crosses the blood--brain barrier, having a direct action on the CNS. Encephalopathy triggered by its toxicity is capable of producing several radiological patterns. After discard infectious encephalitis, it is of utmost importance to consider tacrolimus--induced encephalopathy -- due to rapid clinical and radiological remission after discontinuing the drug.
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Neilan, P. T., and D. Urbine. "Contrast Induced Encephalopathy Mimicking Subarachnoid Hemorrhage." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6640.

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Pradeaux, laurent, Nabil Bendjazia, marie Percot-Blondy, loic Fritsch, maud Sordet, sandra Pochelu, and daniela Behrendt. "P502 Yersinia enterolitica infection with encephalopathy." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.838.

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Windradi, Choirina, Iswan Abbas Nusi, Poernomo Boedi Setiawan, Herry Purbayu, Titong Sugihartono, Ummi Maimunah, Ulfa Kholili, et al. "Liver Diet in Hepatic Encephalopathy Patients." In International Meeting on Regenerative Medicine. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007322504200424.

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Delfim, William de Souza, Nayara Christina de Lima Curti, Marília Pires de Souza e. Silva, Lorena Dias Araújo, Indianara Keila Pastorio, Francine de Paula Roberto Domingos, Sayuri Aparecida Hirayama, Rafael de Almeida, Raquel de Mattos Filgueiras, and Rafael Batista João. "The diagnostic challenge of Hashimoto’s Encephalopathy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.579.

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Introduction: The diagnosis of Hashimoto Encephalopathy (HE) is generally considered in patients with a wide range of neurological symptoms, accompanied by normal or nonspecific findings on magnetic resonance imaging and CSF, normal thyroid function or mild hypothyroidism, increased serum levels of thyroid peroxidase antibodies, and clinical response to steroids. Case report: We attended a 76-year-old patient, brought by lowering the level of consciousness 3 days ago, insidiously. Neurological exam: did not obey commands, and only said incomprehensible sounds. Myoclonus in upper limbs and random multidirectional movements of the eyes with horizontal nystagmus, rapid phase to the left. Cranial tomography had only signs of microangiopathy. Electroencephalogram: diffuse slow waves, with no signs of status epilepticus. Laboratory tests: there were increased protein in CSF (107mg/dl) and Anti-TPO serum (>1000 U/ml) levels, without other specific alterations. After these results, therapy with Methylprednisolone 1g/day for 5 days, and Levothyroxine, were chosen. There was a gradual improvement in the neurological condition from the 3rd day of treatment. Conclusion: immediate recognition of Hashimoto encephalopathy is important. Although the pathogenesis is unknown, the disorder is treatable. This entity should always be remembered for the proper direction of therapeutic approaches, thus enabling better outcomes to the patient.
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Espinel, J., and E. Pinedo. "WERNICKE ENCEPHALOPATHY AFTER INTRAGASTRIC BALLOON PLACEMENT." In ESGE Days 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1745352.

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Barbosa, Mateus Gonçalves de Sena, Ghaspar Gomes de Oliveira Alves Francisco, Rafaela Luiza Vilela de Souza, João Marcos Alcântara de Souza, and Nicollas Nunes Rabelo. "Chronic traumatic encephalopathy in military and sportsists: a factual problem?: a systematic review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.324.

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Background: Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease linked to tau protein associated with recurrent brain trauma, clinically marked by mood, personality, cognitive and behavioral changes. Objectives: The objective of the study was to demonstrate whether athletes and military personnel can really be victims of CTE and to elucidate this same pathology. Design and setting: This is a systematic review, based on the PRISMA guidelines and a literature review with a summary of the evidence found. Methods: Articles were selected, published from 1934 to 2020, in PubMed and Scielo using the descriptors: “chronic traumatic encephalopathy”, “cerebral concussion”, “players”, “boxers”, “athletes” and “military”. Inclusion criteria were: studies available in English, Spanish and Portuguese published, with randomized clinical trial, cohort study or meta-analysis. Results: In 52 articles, 14 were selected for qualitative synthesis in the results table that addresses chronic traumatic encephalopathy in football, soccer and rugby players, boxers and the military. Neuropathologically, CTE is characterized by cerebral atrophy, a pelvic septum cavity with fenestrations, dense diffuse immunoreactive inclusions and a TDP-43 proteinopathy. Microscopically, there are extensive neurofibrillary tangles and spindle-shaped and filiform neurites throughout the brain. Conclusions: American football players, boxers and military men are more likely to trigger CTE, due to the constant mechanical shocks from their heads. The most frequent clinical manifestations were: headache, aggression, dementia, executive dysfunction and suicide. CTE is definitely diagnosed only at autopsy.
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Mohammedzein, A., J. Kimbugwe, R. Hazam, O. Salh, and M. Patel. "Reversible Decerbrate Posturing Due to Hepatic Encephalopathy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5153.

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Reports on the topic "Encephalopaty"

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Milani, Christina, and Nafisa M. Jadavji. Chronic Traumatic Encephalopathy: Connecting Mechanisms to Diagnosis and Treatment. Journal of Young Investigators, September 2017. http://dx.doi.org/10.22186/jyi.33.4.83-86.

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Michael Scolaro, Michael Scolaro. Targeting the brain with Curcumin: Can we treat Chronic Traumatic Encephalopathy? Experiment, September 2017. http://dx.doi.org/10.18258/10004.

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Wang, Jiahe. Efficacy and safety of fenfluramine for developmental and epileptic encephalopathy: Findings from Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0089.

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Cheng, Junxiong, Yafang Chen, Wenfu Cao, and Guoqing Zuo. Is rifaximin better than non-absorbable disaccharide in the treatment of hepatic encephalopathy? A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0094.

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Liang, Xiao, Lihong Wen, Yifang Wu, Yanmin Hao, Shaobo Wang, and Xiaoyu Hu. Retention enema with Traditional Chinese Medicine for hepatic encephalopathy: A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0107.

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Hu, Yang Yang, Xing Zhang, Yue Luo, and Yadong Wang. Systematic review and Meta analysis of the efficacy and safety of rifaximin in the prevention and treatment of hepatic encephalopathy. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, February 2023. http://dx.doi.org/10.37766/inplasy2023.2.0061.

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Review question / Objective: P：Liver cirrhosis patients with risk factors associated with HE attack;HE patients caused by chronic liver diseases represented by cirrhosis. I: Rifaximin treatment. C: Other drugs or placebo. O：HE incidence; HE improvement; All-cause mortality; Blood ammonia level; PSE index; mental state; NCT-A; NCT-B; Adverse events. Condition being studied: Hepatic encephalopathy(HE) is a neuropsychiatric disorder syndrome based on metabolic disorders, which is caused by severe acute and chronic liver dysfunction or various abnormalities of portosystemic shunt (hereinafter referred to as portosystemic shunt). The research data shows that the prevalence of OHE in patients with cirrhosis is 10-14%, and the prevalence of HE in patients with decompensated cirrhosis is 16-21%. HE can lead to 60-80% of patients with liver cirrhosis with mild cognitive impairment, affecting their ability of daily life and quality of life. When OHE occurs, the one-year mortality rate of patients with liver cirrhosis is 64%, which brings a heavy economic burden to patients and public health resources. Therefore, the prevention and early management of HE is very important.
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Caughey, Byron, and David Kocisko. High-Throughput Screening of Compounds for Anti-Transmissible Spongiform Encephalopathy Activity Using Cell-Culture and Cell-Free Models and Infected Animals. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada475121.

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Zhao, kehong, Guangjin Zhou, Wenxiao Ma, Zixuan Ou, rui Xiao, and jiaqi Feng. Acupuncture Combined with Hyperbaric Oxygen in The Treatment of Delayed Encephalopathy after Acute Carbon Monoxide Poisoning：A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0057.

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