scholarly journals The Association between Hepatic Encephalopathy and Diabetic Encephalopathy: The Brain-Liver Axis

2021 ◽  
Vol 22 (1) ◽  
pp. 463
Author(s):  
So Yeong Cheon ◽  
Juhyun Song
Keyword(s):  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Cognitive Dysfunction ◽  
Motor Impairment ◽  
Depressive Mood ◽  
Diabetic Encephalopathy ◽  
Significant Evidence ◽  
Motor Disturbance ◽  
The Relationship ◽  
The Brain

Hepatic encephalopathy (HE) is one of the main consequences of liver disease and is observed in severe liver failure and cirrhosis. Recent studies have provided significant evidence that HE shows several neurological symptoms including depressive mood, cognitive dysfunction, impaired circadian rhythm, and attention deficits as well as motor disturbance. Liver disease is also a risk factor for the development of diabetes mellitus. Diabetic encephalopathy (DE) is characterized by cognitive dysfunction and motor impairment. Recent research investigated the relationship between metabolic changes and the pathogenesis of neurological disease, indicating the importance between metabolic organs and the brain. Given that a diverse number of metabolites and changes in the brain contribute to neurologic dysfunction, HE and DE are emerging types of neurologic disease. Here, we review significant evidence of the association between HE and DE, and summarise the common risk factors. This review may provide promising therapeutic information and help to design a future metabolic organ-related study in relation to HE and DE.

scholarly journals Impaired brain glymphatic flow in a rodent model of chronic liver disease and minimal hepatic encephalopathy

2017 ◽  
Author(s):  
Anna Hadjihambi ◽  
Ian F. Harrison ◽  
Natalia Arias ◽  
Rocío Gallego-Durán ◽  
Patrick S. Hosford ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Chronic Liver Disease ◽  
Minimal Hepatic Encephalopathy ◽  
Brain Regions ◽  
Chronic Liver ◽  
Waste Products ◽  
Cognitive Behavioural ◽  
Contrast Enhanced ◽  
The Brain

AbstractNeuronal function is exquisitely sensitive to alterations in extracellular environment. In patients with hepatic encephalopathy (HE), accumulation of metabolic waste products and noxious substances in the interstitial fluid of the brain may contribute to neuronal dysfunction and cognitive impairment. In a rat model of chronic liver disease, we used an emerging dynamic contrast-enhanced MRI technique to assess the efficacy of the glymphatic system, which facilitates clearance of solutes from the brain. We identified discrete brain regions (olfactory bulb, prefrontal cortex and hippocampus) of altered glymphatic flow, which aligned with cognitive/behavioural deficits. Although the underlying pathophysiological mechanisms remain unclear, this study provides the first experimental evidence of impaired glymphatic clearance in HE.

scholarly journals Systemic inflammation and delirium: important co-factors in the progression of dementia

2011 ◽  
Vol 39 (4) ◽  
pp. 945-953 ◽  
Author(s):  
Colm Cunningham
Keyword(s):  
Cognitive Dysfunction ◽  
Systemic Inflammation ◽  
Sickness Behaviour ◽  
Inflammatory Conditions ◽  
Current Review ◽  
Nervous System Function ◽  
Ad Alzheimer’S Disease ◽  
The Relationship ◽  
The Brain ◽  
Precise Role

It is widely accepted that inflammation plays some role in the progression of chronic neurodegenerative diseases such as AD (Alzheimer's disease), but its precise role remains elusive. It has been known for many years that systemic inflammatory insults can signal to the brain to induce changes in CNS (central nervous system) function, typically grouped under the syndrome of sickness behaviour. These changes are mediated via systemic and CNS cytokine and prostaglandin synthesis. When patients with dementia suffer similar systemic inflammatory insults, delirium is a frequent consequence. This profound and acute exacerbation of cognitive dysfunction is associated with poor prognosis: accelerating cognitive decline and shortening time to permanent institutionalization and death. Therefore a better understanding of how delirium occurs during dementia and how these episodes impact on existing neurodegeneration are now important priorities. The current review summarizes the relationship between dementia, systemic inflammation and episodes of delirium and addresses the basic scientific approaches currently being pursued with respect to understanding acute cognitive dysfunction during aging and dementia. In addition, despite there being limited studies on this subject, it is becoming increasingly clear that infections and other systemic inflammatory conditions do increase the risk of AD and accelerate the progression of established dementia. These data suggest that systemic inflammation is a major contributor to the progression of dementia and constitutes an important clinical target.

scholarly journals A Look into Liver Mitochondrial Dysfunction as a Hallmark in Progression of Brain Energy Crisis and Development of Neurologic Symptoms in Hepatic Encephalopathy

2020 ◽  
Vol 9 (7) ◽  
pp. 2259 ◽  
Author(s):  
Elena Kosenko ◽  
Lyudmila Tikhonova ◽  
Gubidat Alilova ◽  
Carmina Montoliu
Keyword(s):  
Hepatic Encephalopathy ◽  
Liver Toxicity ◽  
Atp Synthesis ◽  
Hepatic Metabolism ◽  
Energy Crisis ◽  
Initial Stage ◽  
Impaired Liver ◽  
The Relationship ◽  
The Brain ◽  
Brain Energy

Background: The relationship between liver disease and neuropathology in hepatic encephalopathy is well known, but the genesis of encephalopathy in liver failure is yet to be elucidated. Conceptually, the main cause of hepatic encephalopathy is the accumulation of brain ammonia due to impaired liver detoxification function or occurrence of portosystemic shunt. Yet, as well as taking up toxic ammonia, the liver also produces vital metabolites that ensure normal cerebral function. Given this, for insight into how perturbations in the metabolic capacity of the liver may be related to brain pathology, it is crucial to understand the extent of ammonia-related changes in the hepatic metabolism that provides respiratory fuel for the brain, a deficiency of which can give rise to encephalopathy. Methods: Hepatic encephalopathy was induced in starved rats by injection of ammonium acetate. Ammonia-induced toxicity was evaluated by plasma and freeze-clamped liver and brain energy metabolites, and mitochondrial, cytoplasmic, and microsomal gluconeogenic enzymes, including mitochondrial ketogenic enzymes. Parameters of oxidative phosphorylation were recorded polarographically with a Clark-type electrode, while other measures were determined with standard fluorometric enzymatic methods. Results: Progressive impairment of liver mitochondrial respiration in the initial stage of ammonia-induced hepatotoxicity and the subsequent energy crisis due to decreased ATP synthesis lead to cessation of gluconeogenesis and ketogenesis. Reduction in glucose and ketone body supply to the brain is a terminal event in liver toxicity, preceding the development of coma. Conclusions: Our study provides a framework to further explore the relationship between hepatic dysfunction and progression of brain energy crisis in hepatic encephalopathy.

scholarly journals Toxic encephalopathy in a clinicl case of polycythemia vera

2020 ◽  
Vol 18 (4) ◽  
pp. 249-255
Author(s):  
P. I. Kuznetsova ◽  
M. M. Tanashyan ◽  
A. A. Kornilova
Keyword(s):  
Hepatic Encephalopathy ◽  
Cerebrovascular Disorders ◽  
Toxic Encephalopathy ◽  
Vein Thrombosis ◽  
Toxic Damage ◽  
Myeloproliferative Diseases ◽  
Paramagnetic Substance ◽  
The Relationship ◽  
The Brain

The article deals with a clinical case description of a female patient with toxic encephalopathy against the background of Ph-negative myeloproliferative diseases. The article discusses symptoms and neuroimaging of hepatic encephalopathy developed as a result of a shunt placed after portal vein thrombosis. The issues of etiology and pathogenesis of hepatic encephalopathy, principles of therapy, as well as the unique clinical picture of nervous system damage in this condition are also discussed. Data on the role of manganese in development of toxic encephalopathy, accumulation of paramagnetic substance in the basal ganglia of the brain and development of extrapyramidal symptoms are presented. The pathogenesis of toxic damage to neurons, increase in their sensitivity to hypoxia, and the relationship with the risk of cerebrovascular disorders and development of chronic cerebral ischemia, contributing to reduction of cognitive functions, are described.

scholarly journals Hepatic Encephalopathy: A Review

2021 ◽  
pp. 89-97
Author(s):  
Savan Kabaria ◽  
Ishita Dalal ◽  
Kapil Gupta ◽  
Abhishek Bhurwal ◽  
Minacapelli Carlos D. ◽  
...  
Keyword(s):  
Amino Acids ◽  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Hospital Costs ◽  
Branched Chain Amino Acids ◽  
Review Article ◽  
Branched Chain ◽  
New Research ◽  
The Brain ◽  
Recurrence Frequency

Hepatic encephalopathy (HE) is a reversible syndrome observed in patients with liver disease. The syndrome is characterised by a spectrum of neuropsychiatric abnormalities resulting from the accumulation of neurotoxic substances in the bloodstream and ultimately in the brain. HE is a huge burden to patients, caregivers, and the healthcare system. Common treatments for HE, including rifaximin and lactulose, have been shown to reduce the risk of recurrence, frequency of hospitalisations, hospital costs, and mortality. New research and therapeutics exist, including faecal transplants and small-molecule therapies such as branched-chain amino acids. This review article provides a general overview of the current understanding of HE.

Grenzenlose Verantwortung

2010 ◽  
Vol 2010 (1) ◽  
pp. 5-22
Author(s):  
Ralf Becker
Keyword(s):  
Personal Freedom ◽  
The Relationship ◽  
The Brain

The article examines the relationship between freedom, guilt and responsibility in Dostojewski’s and Sartre’s works. Both attribute a great measure of personal freedom to man. Therefore, they do not tolerate excuses. Whoever is free, carries responsibility and gets caught up in guilt. Dostojewski’s focus is mainly on guilt, Sartre’s is on responsibility. They share the conviction that we can delegate responsibility for our actions or our way of living neither to a whole, of which we are a part, like society (the ,milieu'), nor to a part, for which we are the whole, like the ,brain' or the ,genes'. In that sense, Dostojewski’s and Sartre’s attempts at an ethic of responsibility also offer convincing arguments against determinism.

EXPERIMENTAL ASSESSMENT OF THE NANOPARTICLES TOXICITY OF NICKEL OXIDE IN TWO SIZES IN THE SUBCHRONIC EXPERIMENT

2018 ◽  
pp. 30-35
Author(s):  
M.P. Sutunkova ◽  
B.A. Katsnelson ◽  
L.I. Privalova ◽  
S.N. Solovjeva ◽  
V.B. Gurvich ◽  
...  
Keyword(s):  
Nickel Oxide ◽  
Nervous Activity ◽  
Equal Mass ◽  
The Body ◽  
Subchronic Toxicity ◽  
Physiological Mechanisms ◽  
Nickel Oxide Nanoparticles ◽  
The Relationship ◽  
The Brain ◽  
Nanoparticles Toxicity

We conducted a comparative assessment of the nickel oxide nanoparticles toxicity (NiO) of two sizes (11 and 25 nm) according to a number of indicators of the body state after repeated intraperitoneal injections of these particles suspensions. At equal mass doses, NiO nanoparticles have been found to cause various manifestations of systemic subchronic toxicity with a particularly pronounced effect on liver, kidney function, the body’s antioxidant system, lipid metabolism, white and red blood, redox metabolism, spleen damage, and some disorders of nervous activity allegedly related to the possibility of nickel penetration into the brain from the blood. The relationship between the diameter and toxicity of particles is ambiguous, which may be due to differences in toxicokinetics, which is controlled by both physiological mechanisms and direct penetration of nanoparticles through biological barriers and, finally, unequal solubility.

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