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Clinical Trial
. 2013 Feb;33(2):272-7.
doi: 10.1038/jcbfm.2012.173. Epub 2012 Nov 21.

Brain magnetic resonance spectroscopy in episodic hepatic encephalopathy

Affiliations
Clinical Trial

Brain magnetic resonance spectroscopy in episodic hepatic encephalopathy

Laia Chavarria et al. J Cereb Blood Flow Metab. 2013 Feb.

Abstract

Brain magnetic resonance (MR) study has shown metabolic abnormalities and changes in water distribution of the brain tissue that may relate to the pathogenesis of hepatic encephalopathy (HE). We designed a study to investigate the disturbances in brain water and metabolites during episodic HE using a 3-T MR scanner. Cirrhotic patients with different grades of HE underwent MR during hospitalization (n=18). The MR was repeated at 6 weeks' follow-up (n=14). The results were compared with those of a group of healthy volunteers (n=8). During episodic HE, brain diffusion-weighted imaging showed a high apparent diffusion coefficient (ADC) (12% to 14%) that decreased during follow-up (-1% to -4%). These disturbances were accompanied by high glutamine (581%), low choline (-31%), and low myo-inositol (-86%) peaks on MR spectroscopy. In overt HE, patients showed high glutamine that decreased during follow-up (-22%). In addition, these patients exhibited a rise in plasma S100 beta and enlargement of brain white-matter lesions. In conclusion, several disturbances detected by MR support the presence of impaired brain water homeostasis during episodic HE. Although astrocytes have a major role in this condition, brain edema during episodic HE may be extracellular and does not appear to be directly responsible for the development of neurologic manifestations.

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Figures

Figure 1
Figure 1
(A) Relative metabolite concentrations in patients with cirrhosis (n=18) and healthy controls (n=8). Metabolites: Gln, glutamine; Glu, glutamate; Ins, myo-inositol; Cho, choline derivates; and NAA, N-acetylaspartate. *P<0.050; (B) Correlation between brain glutamine/creatine ratio (Gln/Cr) and the hepatic encephalopathy (HE) grade determined at the time of the first magnetic resonance (MR) examination.
Figure 2
Figure 2
Follow-up of brain glutamine (Gln/Cr) in relation to the hepatic encephalopathy (HE) severity at first magnetic resonance (MR) study. *P<0.050. Cr, creatine; Gln, glutamine.
Figure 3
Figure 3
(A) Apparent diffusion coefficient values (ADC, in μm2/s) in patients with different grades of hepatic encephalopathy (HE) (in gray, n=18) and controls (ctrl, in white, n=8) in two different regions. The mean of each group is marked by a dash. *P<0.050; (B) Follow-up of ADC values (in μm2/s) in patients with cirrhosis (n=12) in two brain regions. At first magnetic resonance (MR) assessment, values in patients without clinical HE are shown as gray circles, whereas patients with low-grade HE (grades I and II) are shown as dark gray circles. Healthy control values are shown to provide a reference for the normal range. *P<0.050.
Figure 4
Figure 4
Among the 15 patients showing white-matter lesions at first magnetic resonance imaging (MRI), the T2 lesion volume was reassessed at follow-up in 9 patients. *P<0.050.
Figure 5
Figure 5
Correlation between the serum S100 beta protein concentration and the hepatic encephalopathy (HE) grade at the time of magnetic resonance (MR) examination.

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