Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy

Department of Gastroenterology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
Hepatology (Impact Factor: 11.06). 04/2006; 43(4):698-706. DOI: 10.1002/hep.21114
Source: PubMed


Brain water may increase in hepatic encephalopathy (HE). Diffusion tensor imaging was performed in patients with cirrhosis with or without HE to quantify the changes in brain water diffusivity and to correlate it with neuropsychological (NP) tests. Thirty-nine patients with cirrhosis, with minimal (MHE) or overt HE, were studied and compared to 18 controls. Mean diffusivity (MD) and fractional anisotropy (FA) were calculated in corpus callosum, internal capsule, deep gray matter nuclei, periventricular frontal, and occipital white matter regions in both cerebral hemispheres. The MD and FA values from different regions in different groups were compared using analysis of variance and Spearman's rank correlation test. In 10 patients with MHE, repeat studies were performed after 3 weeks of lactulose therapy to look for any change in MD, FA, and NP scores. Significantly increased MD was found with insignificant changes in FA in various regions of brain in patients with MHE or HE compared with controls, indicating an increase in interstitial water in the brain parenchyma without any microstructural changes. A significant correlation was found between MD values from corpus callosum, internal capsule, and NP test scores. After therapy, MD values decreased significantly and there was a corresponding improvement in NP test scores. Further analysis showed that MD values were different for different grades of minimal or overt HE. In conclusion, the increase in MD with no concomitant changes in FA in cirrhosis with minimal or early HE indicates the presence of reversible interstitial brain edema.

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Available from: Piyush Ranjan, Sep 03, 2014
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    • "Several cerebral DWI studies have been undertaken in patients with cirrhosis, but the results are inconsistent, primarily because the cohorts studied have been small and heterogeneous , particularly in relation to the severity of the liver disease and the degree of neuropsychiatric impairment, which was variously assessed, and the MR techniques which were not standardized (Kale et al. 2006; Khalek et al. 2014; Lodi et al. 2004; Sugimoto et al. 2008). Thus, currently the consensus appears to be that while studies using structural and functional cerebral imaging techniques have undoubtedly helped unravel the pathophysiology of HE, they are not thought to offer anything diagnostically (Berding et al. 2009; Grover et al. 2006). "
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    ABSTRACT: Cerebral magnetic resonance imaging was undertaken, at 3 Tesla field strength, employing magnetization transfer (MT) and diffusion-weighted imaging (DWI) sequences, in 26 patients with well-compensated cirrhosis, free of overt hepatic encephalopathy. Results were compared to those from 18 aged-matched healthy volunteers. Cerebral magnetization transfer ratios (MTR) were reduced in the frontal white matter, caudate, putamen and globus pallidus in patients with cirrhosis, compared to healthy controls, while the apparent diffusion coefficients (ADC) on DWI were significantly increased in the genu and body of the corpus callosum. An association between previous excessive alcohol consumption and both MTR and ADCs was noted, but this association was lost when controls were exercised for the severity of liver disease and psychometric impairment on multivariate analysis. Eight (31 %) of the 26 patients had impaired psychometric performance consistent with a diagnosis of minimal hepatic encephalopathy. No statistically significant difference in regional cerebral MTRs or ADCs was found in relation to neuropsychiatric status, although there was a trend towards lower MTRs in patients with impaired psychometric performance. The alterations in MTR and ADC in the patients with functionally compensated cirrhosis are compatible with theories governing the genesis of hepatic encephalopathy, including changes in astrocyte membrane permeability, with subsequent redistribution of macromolecules.
    Full-text · Article · Aug 2015 · Metabolic Brain Disease
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    • "GalN ↑/↓ c ↑ a (Cauli et al. 2011) Human: CLF ↓ ↑ ↓ ↑ ↓ ↑ ↑ (Rose et al. 1999; Cordoba et al. 2001; Lodi et al. 2004; Kale et al. 2006; Shah et al. 2008; Nath et al. 2008; Chavarria et al. 2011) ACLF ≈ ↓ ↑ (Nath et al. 2008) ALF ↓ ≈ ↓ ↓ ↑ (Ranjan et al. 2005; Rai et al. 2008; Saksena et al. 2008) CLF chronic liver failure, ACLF acute-on-chronic liver failure, ALF acute liver failure Animal model: PCA portocava anastomosis, BDL bile-duct ligation, LPS lipopolysaccharides, HAL hepatic artery ligation, HA hyperammonemia by ammonia infusion, Ac acetate, GalN galactosamine injection MRI: T1 T1 relaxation time, T2 T2 relaxation time, MTR magnetic transfer ratio, ADC apparent diffusion coefficient, MD mean diffusivity, FA fractional anisotropy, CS spherical anisotropy a Quantification by no MR technique b Results with discrepancies depending on the BDL studies c Changes depending of the studied region Metab Brain Dis brain tissue density. This is worsen in patients with hepatic encephalopathy history and persisted after liver transplantation (Guevara et al. 2011; Iwasa et al. 2012). "
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    ABSTRACT: Brain alterations such as hepatic encephalopathy or brain edema are usually associated with liver failure. The mechanisms that lead to the generation of edema seem to be different depending on the course of liver failure (acute, chronic or acute-on-chronic liver failure). Several neuroimaging methods allow a non-invasive assessment of brain alterations in liver failure. Magnetic resonance has gained more interest due to the ability of giving information about cerebral metabolism using spectroscopy, water distribution by diffusion methods or neuronal connectivity by means of resting state magnetic resonance. These techniques have been applied to experimental models and patients with liver failure to elucidate cerebral pathways involved in the pathogenesis of hepatic encephalopathy. In the future, the development of new magnetic resonance implementations will generate handy tools for the study of the brain and get better understanding of the mechanisms that take place in liver failure. This could be useful for the early diagnosis, as well as for the design of new treatments for cerebral complications of liver failure.
    Full-text · Article · Nov 2013 · Metabolic Brain Disease
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    • "low-grade interstitial brain edema (Kale et al. 2006), whereas acute liver failure causes intracellular edema that can be severe and lead to brain herniation (Rai et al. 2008). In conventional MR techniques, brain water changes are reflected as an increase in signal intensity on fast-FLAIR imaging in periventricular regions, and as focal white matter lesions or lesions along the corticospinal tract (Rovira et al. 2008). "
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    ABSTRACT: Liver transplantation (LT) candidates experience frequently episodic or persistent hepatic encephalopathy. In addition, these patients can exhibit neurological comorbidities that contribute to cognitive impairment in the pre-transplant period. Assessment of the respective contribution of hepatic encephalopathy or comorbidities in the cognitive manifestations is critical to estimate the neurological benefits of restoring liver function. Magnetic resonance imaging and spectroscopy are useful to assess the impact of liver failure or comorbidities. This assessment is critical to decide liver transplant in difficult cases. In the early postoperative period, LT is commonly complicated by a confusional syndrome. The possible role of persisting hepatic encephalopathy in its development has not been clearly established. The origin is usually considered multifactorial and relates to complications following LT, such as infections, rejection, primary liver dysfunction, immunosuppressors, etc.… The diagnosis and treatment is based in the recognition of comorbidities and optimal care of metabolic disturbances. Several studies have demonstrated recovery of cognitive function after LT in patients that have exhibited hepatic encephalopathy. However, some deficits may persist specifically among patients with persistent HE. Other factors present before LT that contribute to a worse neuropsychological outcome after LT are diabetes mellitus and alcohol consumption. Long-term after LT, cognitive function may worsen in relation to vascular risk factors.
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