Quantitative cerebral water content mapping in hepatic encephalopathy

Shah, N. Jon; Neeb, Heiko; Kircheis, G.; Engels, Patrick; Häussinger, Dieter; Zilles, Karl

doi:10.1016/j.neuroimage.2008.02.057

Cited by 121 publications

(108 citation statements)

References 40 publications

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“…A study in humans with different grades of HE demonstrated a significant increase of water content in white matter that correlated with the severity of HE. No such relationship was established for gray matter (Shah et al, 2008). These results suggest that fibrous astrocytes (white matter) are more susceptible to swelling than protoplasmic astrocytes (gray matter), and that white matter is more amenable to treatment.…”

Section: White and Gray Matter: Residence To Different Types Of Astromentioning

confidence: 71%

“…However, with more advanced, highly sensitive MRI T 2 -weighted sequences (ex. diffusion-weighted imaging (DWI) and magnetization transfer ration (MTR)), there is increasing evidence that brain edema is present in CLD patients (Córdoba et al, 2001, Häussinger, 2006, Kale et al, 2006, McPhail et al, 2012, Rovira et al, 2002, Shah et al, 2008and Sugimoto et al, 2008. MRI provides a good contrast between soft tissues, based on their water content.…”

Section: Evidence Of Brain Edema In Alf and Cldmentioning

confidence: 99%

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Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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Section: White and Gray Matter: Residence To Different Types Of Astromentioning

confidence: 71%

Section: Evidence Of Brain Edema In Alf and Cldmentioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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“…This means that any differences in concentrations and/or extent of labeling when comparing sham þ MSO vs. sham þ vehicle and þ . Under normal conditions, the majority of 15 N-ammonia taken up from blood reacts rapidly with glutamate, forming mono-labeled [5][6][7][8][9][10][11][12][13][14][15] N]glutamine in a reaction catalyzed by glutamine synthetase (GS), which in brain is found only in astrocytes. 5 Figure 2); double-labeling was low and unaffected by MSO (Table 1).…”

Section: Resultsmentioning

confidence: 99%

Effect of Glutamine Synthetase Inhibition on Brain and Interorgan Ammonia Metabolism in Bile Duct Ligated Rats

Fries

Dadsetan

Keiding

et al. 2013

J Cereb Blood Flow Metab

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Ammonia has a key role in the development of hepatic encephalopathy (HE). In the brain, glutamine synthetase (GS) rapidly converts blood-borne ammonia into glutamine which in high concentrations may cause mitochondrial dysfunction and osmolytic brain edema. In astrocyte-neuron cocultures and brains of healthy rats, inhibition of GS by methionine sulfoximine (MSO) reduced glutamine synthesis and increased alanine synthesis. Here, we investigate effects of MSO on brain and interorgan ammonia metabolism in sham and bile duct ligated (BDL) rats. Concentrations of glutamine, glutamate, alanine, and aspartate and incorporation of 15 NH 4 þ into these amino acids in brain, liver, muscle, kidney, and plasma were similar in sham and BDL rats treated with saline. Methionine sulfoximine reduced glutamine concentrations in liver, kidney, and plasma but not in brain and muscle; MSO reduced incorporation of 15 NH 4 þ into glutamine in all tissues. It did not affect alanine concentrations in any of the tissues but plasma alanine concentration increased; incorporation of 15 NH 4 þ into alanine was increased in brain in sham and BDL rats and in kidney in sham rats. It inhibited GS in all tissues examined but only in brain was an increased incorporation of 15 N-ammonia into alanine observed. Liver and kidney were important for metabolizing blood-borne ammonia.

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“…Recent publications have demonstrated the importance of brain white matter changes (volume, biochemically, physiologically) in association with the onset of hepatic encephalopathy (HE) in patients with chronic liver disease [10,11]. Furthermore, we have previously demonstrated white matter as a more amenable area to treatment and possibly a new therapeutic target [12].…”

Section: Introductionmentioning

confidence: 97%

Neuropathological changes in the brain of pigs with acute liver failure

Kristiansen

Lindal

Myreng

et al. 2010

Scandinavian Journal of Gastroenterology

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Kristiansen, R.G. et al., 2010. Neuropathological changes in the brain of pigs with acute liver failure. Scandinavian journal of gastroenterology, 45(7-8) ABSTRACTObjective. Cerebral edema is a serious complication of acute liver failure (ALF), which may lead to intracranial hypertension and death. An accepted tenet has been that the blood-brain barrier is intact and that brain edema is primarily caused by a cytotoxic etiology due to hyperammonemia. However, the neuropathological changes in ALF have been poorly studied. Using a well characterized porcine model we aimed to investigate ultrastructural changes in the brain from pigs suffering from ALF. Materials and methods. Sixteen female Norwegian Landrace pigs weighing 27-35 kg were randomised into two groups: ALF (n = 8) and sham operated controls (n = 8). ALF was induced with an end-to-side portacaval shunt followed by ligation of the hepatic arteries. Biopsies were harvested from three different areas of the brain (frontal lobe, cerebellum, and brain stem) following eight hours of ALF and analyzed using electron microscopy. Results. Profound perivascular and interstitial edema were found in all three areas. Disruption of pericytic and astrocytic processes were seen, reflecting breakdown/lesion of the blood-brain barrier in animals suffering from ALF. Furthermore, neurons and axons were edematous and surrounded by vesicles. Severe damage to Purkinje neuron (necrosis) and damaged myelin were seen in the cerebellum and brain stem, respectively. Biopsies from sham operated animals were normal. Conclusions. Our data support the concept that vasogenic brain edema plays an important role in the development of intracranial hypertension in pigs with ALF.

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Quantitative cerebral water content mapping in hepatic encephalopathy

Cited by 121 publications

References 40 publications

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Effect of Glutamine Synthetase Inhibition on Brain and Interorgan Ammonia Metabolism in Bile Duct Ligated Rats

Neuropathological changes in the brain of pigs with acute liver failure

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