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: 11.19). 04/2006; 43(4):698-706. DOI: 10.1002/hep.21114
Source: PubMed

ABSTRACT 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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    • "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.
    Metabolic Brain Disease 11/2013; DOI:10.1007/s11011-013-9452-9 · 2.40 Impact Factor
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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.
    Metabolic Brain Disease 11/2012; 28(2). DOI:10.1007/s11011-012-9350-6 · 2.40 Impact Factor
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    • "The association between MD and memory function was slightly stronger on the right side in agreement with another recent large study (van Norden et al., 2012). A higher MD in the gray matter tissue may reflect increased extracellular fluid (Kale et al., 2006), but it is uncertain which specific histopathological substrate is reflected by a higher MD in the hippocampus. From autopsy studies it is known that the accumulation of intraneuronal tau occurs in the hippocampus from midlife onward (Braak and Braak, 1997). "
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    ABSTRACT: Hippocampal atrophy on MRI and changes in diffusion tensor imaging (DTI) measures of the hippocampus have been reported in patients with Alzheimer's disease. We examined the association between hippocampal volumes, DTI measures of the hippocampus and memory performance in 892 non-demented persons (age≥55years) across different age groups. Hippocampal volume was segmented on 3D volumetric MRI scans. The segmentations were co-registered to mean diffusivity (MD) and fractional anisotropy (FA) maps to yield mean hippocampal MD and FA measurements. Higher MD of the hippocampus was associated with impaired verbal memory performance. In all persons ≥55years, a higher MD of the hippocampus was associated with a worse memory performance. Hippocampal volumes were very weakly positively associated with delayed recall and only in persons >65years. FA of the hippocampus was not associated with memory performance. Follow-up studies will be needed to determine whether higher MD of hippocampus at younger ages could be an earlier marker of incident Alzheimer's disease than hippocampal volume.
    NeuroImage 08/2012; 63(4):1782-9. DOI:10.1016/j.neuroimage.2012.08.067 · 6.36 Impact Factor
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