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

✍ Scribed by Ravindra A. Kale; Rakesh K. Gupta; Vivek A. Saraswat; Khader M. Hasan; Richa Trivedi; Asht M. Mishra; Piyush Ranjan; Chandra M. Pandey; Ponnada A. Narayana

• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 391 KB
• Volume: 43
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.21114

✦ Synopsis

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. (HEPATOLOGY 2006;43:698-706.)

C erebral edema (CE) is a well-known feature of acute liver disease; however, recently it has also been implicated in chronic liver disease. 1,2 CE in chronic liver disease differs from that in acute liver failure in terms of the temporality of disease. In the former, there is sufficient time for effective compensation and stabilization of osmolyte shift to counteract the osmotic imbalance induced by intra-astrocytic accumulation of glutamine, whereas in the later, evolution of the syndrome is more rapid and does not allow the system to compensate for metabolic changes. 3 CE in acute liver failure is cytotoxic, 4 whereas in chronic liver disease, lowgrade CE is associated with Alzheimer type II change. Magnetic resonance (MR) imaging studies including MR spectroscopy, magnetization transfer (MT), and diffusion-weighted imaging (DWI) have improved our understanding of basic neuroanatomical and pathophysiological alterations in patients with hepatic encephalopathy (HE). High signal intensity in the globus pallidus, putamen, and portions of the internal capsule on T 1 -weighted imaging along with brain atrophy, particularly in frontal lobes, has been described in 50% to 88% of patients with liver cirrhosis and HE. Although various causes have been proposed for this hyperintensity, deposition of manganese is regarded as the most likely explanation, 12 with no direct correlation of pallidal hyperintensity and grade of encephalopathy.