Minimal hepatic encephalopathy in patients with liver cirrhosis: Magnetic resonance spectroscopic brain findings versus neuropsychological changes

Hassan, Elham Ahmed; El-Rehim, Abeer S. Abd; Seifeldein, Gehan S.; Shehata, Ghaydaa A.

doi:10.1016/j.ajg.2014.09.003

Cited by 13 publications

(10 citation statements)

References 32 publications

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“…Thus, we used Glx to represent both glutamate and glutamine. According to previous studies, excessive brain glutamine was found in hepatic encephalopathy [6]. Second, we did not compare the differences in metabolites on MRS between chronic HSJ patients with PSE and patients with hepatic encephalopathy.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, many patients develop PSE due to the portal-systemic shunting, which is frequently misdiagnosed as dementia, depression, or other psychiatric disorder [1]. Furthermore, chronic HSJ patients with covert PSE are usually clinically undetectable [1, 6]. …”

Section: Introductionmentioning

confidence: 99%

“…Magnetic resonance spectroscopy (MRS) has been used to detect abnormal metabolism in the brain. Previous studies showed increased glutamine levels in patients with hepatic encephalopathy [6, 8]. Recently, abnormal oxidation and carbohydrate fermentation were also found [9, 10].…”

Section: Introductionmentioning

confidence: 99%

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Magnetic Resonance Spectroscopy for Evaluating Portal-Systemic Encephalopathy in Patients with Chronic Hepatic Schistosomiasis Japonicum

Mei

Qiang

et al. 2016

PLoS Negl Trop Dis

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Portal-systemic encephalopathy (PSE) is classified as type B hepatic encephalopathy. Portal-systemic shunting rather than liver dysfunction is the main cause of PSE in chronic hepatic schistosomiasis japonicum (HSJ) patients. Owing to lack of detectable evidence of intrinsic liver disease, chronic HSJ patients with PSE are frequently clinically undetected or misdiagnosed, especially chronic HSJ patients with covert PSE (subclinical encephalopathy). In this study, we investigated whether magnetic resonance spectroscopy (MRS) could be a useful tool for diagnosing PSE in chronic HSJ patients. Magnetic resonance (MR) T1-weighted imaging, diffusion-weighted imaging, and MRS were performed in 41 chronic HSJ patients with suspected PSE and in 21 age-matched controls. The T1 signal intensity index (T1SI) and apparent diffusion coefficient (ADC) value were obtained in the Globus pallidus. Liver function was also investigated via serum ammonia and liver function tests. Higher T1SI and ADC values, increased lactate and glutamine levels, and decreased myo-inositol were found in the bilateral Globus pallidus in chronic HSJ patients with PSE. No significantly abnormal serum ammonia or liver function tests were observed in chronic HSJ patients with PSE. On the basis of these findings, we propose a diagnostic procedure for PSE in chronic HSJ patients. This study reveals that MRS can be useful for diagnosing PSE in chronic HSJ patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Magnetic Resonance Spectroscopy for Evaluating Portal-Systemic Encephalopathy in Patients with Chronic Hepatic Schistosomiasis Japonicum

Mei

Qiang

et al. 2016

PLoS Negl Trop Dis

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“…При минимальной ПЭ она проявляется преимущественно нарушениями абстрактного мышления и общим негрубым снижением когнитивных функций без нарушений памяти, интеллекта, речи, способности к обучению, которые остаются сохранными в течение длительного времени [18,19]. У некоторых больных с печеночной недостаточностью в течение ряда лет выявляют лишь нарушения высших функций мозга без какой-либо иной неврологической симптоматики [20].…”

Section: клиникаunclassified

Hepatic encephalopathy

Никонов¹,

Аксенов²

2017

Dok. gastroenterol.

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Печеночная энцефалопатия (ПЭ)-это потенциально обратимый синдром нарушения функций головного мозга у больных с прогрессирующей печеночной недостаточностью. Даже в самой мягкой форме ПЭ снижает качество жизни, обусловленное состоянием здоровья, и является фактором риска эпизодов тяжелой ПЭ. Механизмы, нарушающие функции головного мозга при печеночной недостаточности, до сих пор полностью не изучены, однако ясно, что они напрямую связаны с печеночной недостаточностью и нарушением обмена аммиака. Наиболее распространенные гипотезы патогенеза отражают роль нейротоксинов, нарушение нейротрансмиссии вследствие метаболических нарушений при печеночной недостаточности, изменение энергетического метаболизма мозга, аминокислотный дисбаланс, системный воспалительный ответ и нарушения проницаемости гематоэнцефалического барьера.

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“…In the US from 2005 to 2009 up to 110000 patients with HE were hospitalized per year [4]. 70-87 % of liver cirrhosis cases are accompanied by latent, or "minimal" HE, while 30-45 % of patients may show symptoms of moderate up to the severe form [5,6], which is accompanied by cerebral edema development, intracranial hypertension (ICH) decompensation and fatal outcome. Approximately 30 % of patients dying in the final stages of liver disease have a signs of severe HE turning into a coma.…”

Section: Introductionmentioning

confidence: 99%

Modern view on hepatic encephalopathy: basic terms and concepts of pathogenesis

Shulyatnikova

Shavrin

2017

Patologìâ

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Background. The problem of acute and chronic forms of hepatic encephalopathy (HE) is not clearly identified among modern problems of hepatology and neuroscience in Ukraine. Despite the significant contribution to the development of lethal complications in patients with liver pathology and long history of the study of this issue, there is still no unified opinion on the links of HE pathogenesis.The aim of this review is to conduct a comprehensive analysis of current data on the spreading and mechanisms of development of HE.HE is a complex of potentially reversible neurocognitive disorders in patients with chronic or acute hepatic failure (ALF). HE is more often a complication of liver cirrhosis and is the second most frequent cause of hospitalization of such patients after ascites. When decompensating liver failure in acute or chronic hepatic pathology in patients severe forms of HE develop, accompanied by a progressive increase in intracranial pressure and the development of coma, which often ends lethal due to poor corrigibility of intracranial hypertension while maintaining hepatogenic neurointoxication. HE is considered as the end result of the accumulation of a number of neurotoxic substances in the brain, among which are ammonia, mercaptans, short chain fatty acids, false neurotransmitters, gamma-aminobutyric acid, manganese. The most popular among the reasons for the development of HE is the neurotoxic theory of ammonia. Ammonia is subjected to detoxification in the liver, turning into urea, a smaller fraction with the participation of glutamine synthetase is used in the synthesis of glutamine in muscles, liver and astrocytes of brain. In case of hepatic dysfunction and/or portosystemic shunting, the concentration of ammonia in blood increases up to 10 times and the main load for its detoxification is shifted to myocytes and astroglia. In ALF glutamine overload of astrocytes occurs with a change in intracellular osmolarity and subsequent edema of astroglia, which is accompanied by the development of cytotoxic edema of the brain. In this case, in astrocytes damaging of mitochondrial respiratory chain occurs and mitochondrial insufficiency develops, as well as processes of nitrosative-oxidative stress and oxidation of astrocytic and neuronal RNA, disruption of gene expression, synthesis of neuro-and gliotransmitters and synaptic plasticity. The increased influx of aromatic amino acids into brain leads to the synthesis of false neurotransmitters, which worsens serotoninergic, GABA-ergic, dopaminergic and glutamatergic neurotransmission. Damage to the components of the blood-brain barrier leads to aggravation of the water imbalance, penetration of hematogenous cytokines, endotoxins and other products of systemic inflammatory reaction into the cerebral parenchyma and development of neuroinflammation, which makes an important contribution to the further progression of cerebral edema.Conclusions: despite a comprehensive study of the problem, many open questions remain in the pathogenesis of HE. Special attention ...

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Minimal hepatic encephalopathy in patients with liver cirrhosis: Magnetic resonance spectroscopic brain findings versus neuropsychological changes

Cited by 13 publications

References 32 publications

Magnetic Resonance Spectroscopy for Evaluating Portal-Systemic Encephalopathy in Patients with Chronic Hepatic Schistosomiasis Japonicum

Magnetic Resonance Spectroscopy for Evaluating Portal-Systemic Encephalopathy in Patients with Chronic Hepatic Schistosomiasis Japonicum

Hepatic encephalopathy

Modern view on hepatic encephalopathy: basic terms and concepts of pathogenesis

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