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  • Portal-systemic encephalopathy  (5)
  • Hepatic encephalopathy  (4)
  • Thiamine deficiency  (3)
  • manganese  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Pathophysiology of alcoholic brain damage: synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 1-8 
    Details
    ISSN: 1573-7365
    Keywords: Alcoholic brain damage ; Ethanol neurotoxicity ; Thiamine deficiency ; Alcoholic liver disease ; Hepatic Encephalopathy ; Cerebral energy deficit ; NMDA receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic alcoholism results in brain damage and dysfunction leading to a constellation of neuropsychiatric symptoms including cognitive dysfunction, the Wernicke-Korsakoff Syndrome, alcoholic cerebellar degeneration and alcoholic dementia. That these clinically-defined entities result from independent pathophysiologic mechanisms is unlikely. Alcohol and its metabolite acetaldehyde are directly neurotoxic. Alcoholics are thiamine deficient as a result of poor diet, gatrointestinal disorders and liver disease. In addition, both alcohol and acetaldehyde have direct toxic effects on thiamine-related enzymes in liver and brain. Alcoholics frequently develope severe liver disease and liver diseaseper se results in altered thiamine homeostasis, in cognitive dysfunction and in neuropathologic damage to astrocytes. The latter may result in the loss of neuron-astrocytic trafficking of neuroactive amino acids and thiamine esters, essential to CNS function. The present review article proposes mechanisms whereby the effects of alcohol, thiamine deficiency and liver disease combine synergistically to contribute to the phenomena of cognitive dysfunction and “alcoholic brain damage”.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991777
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  • 2
    Electronic Resource
    Electronic Resource
    Portacaval Anastomosis Results in More Widespread Alterations of Cerebral Metabolism in Old Versus Young Adult Rats: Implications for Post-Shunt Encephalopathy (1998)
    Springer
    Metabolic brain disease 13 (1998), S. 69-78 
    Details
    ISSN: 1573-7365
    Keywords: Hepatic Encephalopathy ; Portal-systemic encephalopathy ; Post-shunt encephalopathy ; Portacaval anastomosis ; Brain glucose metabolism ; Age-related changes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Treatment of portal hypertension by portal decompressive surgery or transjugular intrahepatic portosystemic stent shunt (TIPS) results in new or worsening episodes of portal-systemic encephalopathy, particularly in older patients. As part of a series of studies to elucidate the pathophysiologic mechanisms responsible for the age-related increased portal-systemic encephalopathy following shunt surgery, local cerebral glucose utilization, a measure of regional brain functional activity, was assessed using the 14C-2-deoxyglucose autoradiographic technique in 2 month-old (young adult) and 24 month-old (old adult) rats following end-to-side portacaval anastomosis. Cerebral glucose utilization was decreased by 22% (p〈0.05) in frontal cortex of 2 month-old rats following portacaval anastomosis. More widespread alterations of glucose utilization, involving frontal and frontoparietal cortices, as well as thalamic structures were observed in the brains of 24 month-old rats following portacaval anastomosis despite blood ammonia concentrations of a comparable magnitude. Decreased cerebral glucose utilization in frontal and frontoparietal cortex of old adult rats following portacaval anastomosis probably results from decreased cerebral energy requirements as a consequence of neurotransmitter-related dysfunction. The greater susceptibility of aging brain to the deleterious effects of portacaval anastomosis is consistent with the higher incidence of encephalopathy in older cirrhotic patients following portacaval anastomosis or TIPS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020683013238
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  • 3
    Electronic Resource
    Electronic Resource
    Neuroactive amino acids in hepatic encephalopathy (1996)
    Springer
    Metabolic brain disease 11 (1996), S. 165-173 
    Details
    ISSN: 1573-7365
    Keywords: Hepatic encephalopathy ; Amino acids ; Glutamate ; GABA ; Taurine ; Endogenous benzodiazepines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is abundant evidence to suggest that alterations of excitatory and inhibitory amino acids play a significant role in the pathogenesis of hepatic encephalopathy (HE) in both acute and chronic liver diseases. Brain glutamate concentrations are reduced in patients who died in hepatic coma as well as in experimental HE, astrocytic reuptake of glutamate is compromised in liver failure and postsynaptic glutamate receptors (both NMDA and non-NMDA subclasses) are concomitantly reduced in density. Recent studies in experimental acute liver failure suggest reduced capacity of the astrocytic glutamate transporter in this condition. Together, this data suggests that neuron-astrocytic trafficking of glutamate is impaired in HE. Other significant alterations of neuroactive amino acids in HE include a loss of taurine from brain cells to extracellular space, a phenomenon which could relate both to HE and to brain edema in acute liver failure. Increased concentrations of benzodiazepine-like compounds have been reported in human and experimental HE. Clinical trials with the benzodiazepine antagonist flumazenil reveal a beneficial effect in some patients with HE; the mechanism responsible for this effect, however, remains to be determined.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02069503
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  • 4
    Electronic Resource
    Electronic Resource
    Densities of binding sites for the “peripheral-type” benzodiazepine receptor ligand3H-PK11195 are increased in brain 24 hours following portacaval anastomosis (1994)
    Springer
    Metabolic brain disease 9 (1994), S. 267-273 
    Details
    ISSN: 1573-7365
    Keywords: Portacaval anastomosis ; Hepatic encephalopathy ; 3H-PK11195 binding ; “Peripheral-type” benzodiazepine receptor ; Astrocyte ; Portal-systemic encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Quantitative receptor autoradiography was used to measure the densities of binding sites for the “peripheral-type” benzodiazepine receptor ligand3H-PK11195 in regions of the rat brain 1, 3, 7 and 28 days following portacaval anastomosis (PCA) and in sham-operated control animals. The results demonstrate that densities of3H-PK11195 binding sites were significantly increased in the cerebral cortex (by 40%, p〈0.05) as early as 24 hours following PCA. In the thalamus significant increases in densities of3H-PK11195 binding sites were seen 3 days after PCA, whereas in brain regions such as the striatum and cerebellum, significant increases in3H-PK11195 binding sites were not evident until 7 days following PCA. By 28 days following PCA increased densities of3H-PK11195 binding sites were well established and widespread throughout the brain. Previous studies demonstrate early increases of brain ammonia following. PCA. PTBRs or their endogenous ligands could play an important role in the early astrocytic response (mitochondrial proliferation, swelling) to ammonia following PCA.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991200
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  • 5
    Electronic Resource
    Electronic Resource
    Manganese toxicity, dopaminergic dysfunction and hepatic encephalopathy (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 259-267 
    Details
    ISSN: 1573-7365
    Keywords: manganese ; hepatic encephalopathy ; MR signal hyperintensity ; globus pallidus ; dopamine D2 receptors ; MAO ; extrapyramidal symptoms
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Patients with chronic liver disease manifest a high incidence (〉75%) of pallidal signal hyperintensity on T1-weighted Magnetic Resonance Imaging (MRI), the intensity of which correlates with blood manganese levels and the presence of extrapyramidal symptoms. A major cause of pallidal hyperintensity on T1-weighted MRI is manganese deposition; chronic manganese intoxication in the absence of liver disease results in pallidal MR signal hyperintensity, in extrapyramidal symptoms and in selective effects on the dopaminergic neurotransmitter system in basal ganglia. Direct measurements in globus pallidus obtained at autopsy from patients with chronic liver disease who died in hepatic coma reveal 2 to 7-fold increases of pallidal manganese and a concomitant loss of dopamine D2 binding sites. Liver transplantation results in normalization of pallidal MR signals and of blood manganese levels. These findings suggest that (1) pallidal MR signal hyperintensity in patients with chronic liver disease is the result of manganese deposition and (2) alterations of dopaminergic function due to the toxic effects of manganese may contribute to the extrapyramidal symptoms in these patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02109357
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  • 6
    Electronic Resource
    Electronic Resource
    Accumulation of manganese and copper in pallidum of cirrhotic patients: role in the pathogenesis of hepatic encephalopathy? (1995)
    Springer
    Metabolic brain disease 10 (1995), S. 353-356 
    Details
    ISSN: 1573-7365
    Keywords: Hepatic encephalopathy ; manganese ; copper ; zinc ; globus pallidus ; liver disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Concentrations of zinc, copper and manganese were measured by atomic absorption spectrometry in samples of globus pallidus obtained at autopsy from 9 patients with chronic liver disease and an equal number of age-matched controls. Manganese concentrations were significantly increased several fold (p〈0.01) in globus pallidus of liver disease patients accompanied by smaller but significant 2-fold increases of copper. Zinc concentrations, on the other hand, were within normal limits. Increased pallidal manganese offers a cogent explanation for the observed T1-weighted MRI signal hyperintensity in pallidum of cirrhotic patients. Increased copper content in brain suggests the existence of common pathophysiologic mechanisms in inherited (Wilson Disease) and acquired hepatocerebral disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02109365
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  • 7
    Electronic Resource
    Electronic Resource
    Alterations of Neurotransmitter-Related Gene Expression in Human and Experimental Portal-Systemic Encephalopathy (1998)
    Springer
    Metabolic brain disease 13 (1998), S. 337-349 
    Details
    ISSN: 1573-7365
    Keywords: Portal-systemic encephalopathy ; hepatic encephalopathy ; ammonia ; manganese ; gene expression ; peripheral-type benzodiazepine receptors ; monoamine oxidase ; serotonin ; neurosteroids ; nitric oxide synthase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Portal-systemic encephalopathy (PSE) is a serious neuropsychiatric condition that results from chronic liver failure and portal-systemic shunting of venous blood. PSE is particularly prevalent following treatment of portal hypertension or ascites by the TIPS procedure. Recent studies both in autopsied brain tissue from PSE patients as well as in experimental animal models of PSE reveal that chronic liver failure results in altered expression of several genes coding for proteins having key roles in the control of neuronal excitability. Such alterations include increased expression of monoamine oxidase (MAO-A isoform), the “peripheral-type” benzodiazepine receptor (PTBR) as well as constitutive, neuronal nitric oxide synthase (nNOS). Such changes result in altered protein expression and in increased degradation of monoamine neurotransmitters, increased synthesis of neurosteroids with inhibitory properties and increased production of nitric oxide (respectively) in brain in chronic liver failure. In the case of PTBR and nNOS, increases in expression result from exposure to ammonia and/or manganese, two neurotoxic agents shown previously to be increased in brain in chronic liver failure. Further elucidation of the consequences of neurotransmitter-related gene expression could identify new pathophysiologic mechanisms and result in new approaches to the prevention of PSE in chronic liver disease in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020641009971
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  • 8
    Electronic Resource
    Electronic Resource
    Cerebrospinal fluid amino acids in relation to neurological status in experimental portal-systemic encephalopathy (1991)
    Springer
    Metabolic brain disease 6 (1991), S. 65-74 
    Details
    ISSN: 1573-7365
    Keywords: Portal-systemic encephalopathy ; hepatic encephalopathy ; amino acids ; glutamine ; GABA ; phenylalanine ; tyrosine ; ammonia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using an indwelling cisterna magna catheter technique, serial CSF samples were analyzed for amino acid content in rats at various stages of portal-systemic encephalopathy resulting from ammonium acetate administration following portacaval anastomosis. Anastomosis alone resulted in increased CSF concentrations of glutamine, tyrosine, phenylalanine, glutamate and alanine. GABA levels, on the other hand were not significantly changed. Onset of severe neurological symptoms following ammonium acetate administration resulted in selectively increased CSF alanine. Other amino acids were not further increased at severe stages of encephalopathy. Increased CSF alanine probably results from increased glutamine transamination in the brains of portacaval shunted rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999904
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  • 9
    Electronic Resource
    Electronic Resource
    Increased cerebrospinal fluid lactate reflects deterioration of neurological status in experimental portal-systemic encephalopathy (1991)
    Springer
    Metabolic brain disease 6 (1991), S. 225-231 
    Details
    ISSN: 1573-7365
    Keywords: Portal-systemic encephalopathy ; hepatic encephalopathy ; lactate ; brain energy metabolism ; CSF cannula technique ; malate-aspartate shuttle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Increased brain and CSF lactate have been described in human and experimental portal-systemic encephalopathy (PSE). Using a recently described cisterna magna catheter technique, CSF lactate was measured in relation to deterioration of neurological status in portacaval shunted rats administered ammonium acetate to precipitate severe PSE. Loss of righting reflex (precoma stage of PSE) was accompanied by 2–3 fold increased CSF lactate and onset of coma by 4-fold increases of lactate (p〈 0.001 compared to either sodium acetate treated portacaval shunted rats or sham-operated controls administered ammonium acetate). The most likely explanation for increased CSF lactate is ammonia-induced inhibition of malate-aspartate shuttle and/or inhibition of tricarboxylic acid cycle flux in brain. Similar mechanisms could be involved in the pathogenesis of PSE in patients with chronic liver disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00996922
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  • 10
    Electronic Resource
    Electronic Resource
    Activities of thiamine-dependent enzymes in two experimental models of thiamine deficiency encephalopathy: 3. Transketolase (1987)
    Springer
    Neurochemical research 12 (1987), S. 305-310 
    Details
    ISSN: 1573-6903
    Keywords: Thiamine deficiency ; thiamine deprivation ; pyrithiamine ; thiamine pyrophosphate ; transketolase ; Wernicke's encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Chronic thiamine deprivation in the rat leads to ataxia, loss of righting reflex and neuropathological damage to lateral vestibular nucleus. Before onset of neurological symptoms, transketolase (TK) activities were found to be selectively reduced by 25% in lateral vestibular nucleus and surrounding pons. Further progression of thiamine deprivation resulted in a generalized reduction in TK activity. Measurement of enzyme activity in the presence of added TPP cofactor in vitro did not lead to normalisation of enzyme activities suggesting loss of apoenzyme. Administration of thiamine to symptomatic thiamine-deprived rats resulted in reversal of neurological symptoms and to normalisation of defective TK activities in less vulnerable structures such as cerebral cortex striatum and hippocampus; reduction of TK activity, however, persisted in brainstem and cerebellar regions. Pyrithiamine treatment results, within 3 weeks, in loss of righting reflex, convulsions and more widespread neuropathological damage compared to that observed following thiamine deprivation. TK activity was found to be significantly decreased before the onset of neurological symptoms in all brain regions and appearance of symptoms was accompanied by more severe reductions of TK. In contrast to chronic thiamine deprivation, TK activities following pyrithiamine treatment were: (i) equally reduced in magnitude in vulnerable and non-vulnerable brain structures, (ii) unchanged following reversal of neurological abnormalities by thiamine administration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00972141
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