Proton magnetic resonance spectroscopy studies on human brain Myo-inositol in hypo-osmolarity and hepatic encephalopathy

Häussinger, Dieter; Laubenberger, Jörg; Dahl, Stephan Vom; Ernst, Thomas; Bayer, S.; Langer, Mathias; Gerok, W.; Hennig, Jürgen

doi:10.1016/0016-5085(94)90552-5

Cited by 393 publications

(273 citation statements)

References 21 publications

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“…6 The most accepted hypothesis for this low-grade brain edema is that astrocytic accumulation of glutamine induces edema as a result of ammonia detoxification. This hypothesis is supported by experimental data showing astrocyte swelling and changes in brain organic osmolytes in models of HE, 7 and by brain proton magnetic resonance spectroscopy studies in patients with liver cirrhosis, which consistently show increases in the glutamine/glutamate signal accompanied by myoinositol depletion, 8 …”

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confidence: 66%

Decreased white matter lesion volume and improved cognitive function after liver transplantation

et al. 2007

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Focal T2-weighted white matter lesions (WML) on brain magnetic resonance imaging (MRI), mimicking those seen in cerebrovascular small-vessel disease described in patients with persistent hepatic encephalopathy, decreased in volume with the improvement of hepatic encephalopathy. This outcome has been interpreted as a decrease in the edema that it is proposed to be involved in the pathogenesis of hepatic encephalopathy. We designed a study to further investigate potential changes in focal WML in the brains of patients with cirrhosis following liver transplantation and to study the relationship between these changes and overall cognitive function. We used MRI to measure the volume of supratentorial focal WML and a neuropsychological examination to assess cognitive function before and after liver transplantation in 27 patients with cirrhosis without signs of overt hepatic encephalopathy. Baseline MRI identified focal T2-weighted lesions in 19 patients (70.3%). The presence of WML was associated with older age but not with vascular risk factors, severity of liver function, or psychometric tests. A significant reduction in lesion volume was observed after liver transplantation (from a median of 1.306 cm 3 to 0.671 cm 3 , P ‫؍‬ 0.001). This decrease correlated with an improvement in an index of global cognitive function (r ‫؍‬ ؊0.663; P < 0.001). This evolution indicates that lesion volume is partially related to a reversible type of tissue damage, which is compatible with brain edema. F ocal white matter lesions (WML) secondary to cerebrovascular small-vessel disease are commonly found in the general population over 60 years of age. 1 In a previous report, we described focal brain WML on T2-weighted images in patients with hepatic encephalopathy (HE). 2 This abnormality, which is radiologically indistinguishable from the features of small-vessel disease or normal aging, was partially reversible with improvements in HE. This evolution pattern contrasts with what occurs in focal WML attributable to small-vessel disease or brain aging, which remain stable or progress in number and size over time, but never decrease. [3][4][5] The most plausible explanation for decreasing the volume of WML with improvement of HE is a decrease in the edema component of WML.There is a large body of evidence indicating an increase in the amount of water in the brain of patients with liver cirrhosis that is related to the development of HE. 6 The most accepted hypothesis for this low-grade brain edema is that astrocytic accumulation of glutamine induces edema as a result of ammonia detoxification. This hypothesis is supported by experimental data showing astrocyte swelling and changes in brain organic osmolytes in models of HE, 7 and by brain proton magnetic resonance spectroscopy studies in patients with liver cirrhosis, which consistently show increases in the glutamine/glutamate signal accompanied by myoinositol depletion, 8

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confidence: 66%

Decreased white matter lesion volume and improved cognitive function after liver transplantation

et al. 2007

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“…8 The majority of therapeutic measures currently in use are therefore directed at reducing blood Abbreviations: HE, hepatic encephalopathy; SHE, subclinical hepatic encephalopathy; ammonia levels, 9-13 mainly by diminishing enteric ammonia OA, L-ornithine-L-aspartate; GS, glutamine synthetase; NCT-A, number connection test A; PSEI, portal systemic encephalopathy index.…”

Section: Although a Slight Improvement Occurred In The Placebomentioning

confidence: 99%

Therapeutic efficacy ofL-ornithine-L-aspartate infusions in patients with cirrhosis and hepatic encephalopathy: Results of a placebo-controlled, double-blind study

et al. 1997

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prandial venous ammonia concentrations in the OAOne hundred twenty-six patients with cirrhosis, hytreated group showed improvements in comparison perammonemia (ú50 mmol/L), and chronic (persistent) with placebo. In addition, venous fasting blood ammonia hepatic encephalopathy (HE), which developed spontaconcentration (P õ .01), mental state gradation (P õ neously without the existence of known precipitating .001), and PSEI (P õ .01), which includes the mental state factors, were enrolled in a randomized, double-blind, gradation, NCT-A time, and postprandial venous ammoplacebo-controlled clinical trial of intravenously adminnia in this trial, improved to a much higher degree in Hepatic encephalopathy (HE) is one of the major complicapresented are based on the total study sample (intent-to-tions of cirrhosis. Five years after the diagnosis of cirrhosis, treat analysis), which included 63 patients in the placebo the probability of developing at least one episode of this spegroup and 63 patients in the OA group. Of the 126 pa-cific form of decompensated cirrhosis is in the range of 26%. 1 tients, 114 met all the criteria for inclusion and com-Once clinical decompensation has occurred, however, the pleted the trial and treatment as outlined in the protocol prognosis (16% 1 to 22% 2 probability of survival at 5 years) (treated-per-protocol analysis). During baseline, the pla-compared with a survival probability of 55% 2 to 70% 1 in circebo and treatment groups were homogeneous with re-rhotic patients without HE is very poor. 1,2 Therefore, prevengard to mental states, NCT-A performance time, fasting tion and effective treatment of HE may have important progvenous blood ammonia levels, and Child-Pugh criteria. nostic implications in cirrhotic patients. Although a slight improvement occurred in the placeboHyperammonemia 3,4 by a variety of postulated mechagroup, NCT-A performance times (P õ .001) and post-nisms 3-8 is felt to be one of the primary pathogenetic factors in the development of HE. 8 The majority of therapeutic measures currently in use are therefore directed at reducing blood Abbreviations: HE, hepatic encephalopathy; SHE, subclinical hepatic encephalopathy; ammonia levels, 9-13 mainly by diminishing enteric ammonia OA, L-ornithine-L-aspartate; GS, glutamine synthetase; NCT-A, number connection test A; PSEI, portal systemic encephalopathy index.production. Otherwise, it is known that liver and muscle play From the 1 Martin-Luther-University Halle-Wittenberg, Department of Internal Median important part within the ammonia detoxification system, cine, Halle;

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“…53 MRS changes observed in HE are reversible after liver transplantation or pharmacological treatment. 35,54,55 8. Correct answer: A ICP measurement is indicated in patients of ALF who have grade 3 or 4 encephalopathy.…”

Section: Correct Answers: B C D and Ementioning

confidence: 99%

Hepatobiliary Quiz (Answers)—14 (2015)

Rathi

Dhiman

2015

Journal of Clinical and Experimental Hepatology

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Proton magnetic resonance spectroscopy studies on human brain Myo-inositol in hypo-osmolarity and hepatic encephalopathy

Cited by 393 publications

References 21 publications

Decreased white matter lesion volume and improved cognitive function after liver transplantation

Decreased white matter lesion volume and improved cognitive function after liver transplantation

Therapeutic efficacy ofL-ornithine-L-aspartate infusions in patients with cirrhosis and hepatic encephalopathy: Results of a placebo-controlled, double-blind study

Hepatobiliary Quiz (Answers)—14 (2015)

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