El-Khashab, M., ElGhonamy, S., Galal, S., Salama, R., Sanour, A. (2012). Study of Brain Changes in Chronic Hepatic Encephalopathy by Using MR Imaging. Afro-Egyptian Journal of Infectious and Endemic Diseases, 2(4), 140-147. doi: 10.21608/aeji.2012.16087
Mohamed N El-Khashab; Salama M ElGhonamy; Sherif M Galal; Rasha I Salama; Adel AL Sanour. "Study of Brain Changes in Chronic Hepatic Encephalopathy by Using MR Imaging". Afro-Egyptian Journal of Infectious and Endemic Diseases, 2, 4, 2012, 140-147. doi: 10.21608/aeji.2012.16087
El-Khashab, M., ElGhonamy, S., Galal, S., Salama, R., Sanour, A. (2012). 'Study of Brain Changes in Chronic Hepatic Encephalopathy by Using MR Imaging', Afro-Egyptian Journal of Infectious and Endemic Diseases, 2(4), pp. 140-147. doi: 10.21608/aeji.2012.16087
El-Khashab, M., ElGhonamy, S., Galal, S., Salama, R., Sanour, A. Study of Brain Changes in Chronic Hepatic Encephalopathy by Using MR Imaging. Afro-Egyptian Journal of Infectious and Endemic Diseases, 2012; 2(4): 140-147. doi: 10.21608/aeji.2012.16087
Study of Brain Changes in Chronic Hepatic Encephalopathy by Using MR Imaging
1Tropical Medicine Department, Faculty of Medicine, Zagazig University,Egypt
2Radiology Department, Faculty of Medicine, Zagazig University,Egypt
Abstract
Background and study aim: Hepatic encephalopathy (HE) reflects a spectrum of neuro-psychiatric abnormalities. The aim of this study was to evaluate MR imaging of the brain in different grades of chronic HE and its correlation with clinical neurological abnormalities. Patients and Methods: Sixty patients were included, 40 patients with chronic HE were divided into group I (GI) chronic persistent HE (n=20), group II (GII) chronic relapsing HE (n=20), another 20 patients with early compensated cirrhosis were chosen as control group (GIII), all patients were subjected to full clinical and laboratory investigations, estimation of serum ammonia and Manganese level in the blood, psychometric tests ,conventional MRI and MRS. Results: A statistically significant increase in serum level of ammonia and manganese in GI (162.155.8 mol/L, 3.350.34 ug/dl, respectively) when compared to other groups. By conventional MRI there was statistically significant increased signal intensity of T1 and T2 in group I compared with other groups. By MRS, there was statistical significant increase of glutamine in GI (3.90.17 pp,) when compared to GII (3.70.13 ppm) & GIII (2.480.3 ppm) and significant reduction of both choline and myinstol among GI 1.980.17 ppm, 2.190.20 ppm, when compared to GII 2.290.17 ppm, 2.740.17 ppm and GIII 2.590.019 ppm, 3.150.11 ppm. Moreover there was significant elevation in signal intensity of T1 corresponding to elevation of serum manganese (2.910.6 ug/dl) and significant elevation of signal intensity in T2 corresponding to elevation of serum ammonia (116.949 mol/L), as well as highly significant positive correlation between serum ammonia and glutamine (r = 0.86) and highly significant negative correlation between serum ammonia and choline (r = -0.42) and myinstol (r = -0.47). Conclusion: Changes in brain metabolites as detected by MRS may be sensitive markers for clinical monitoring of brain dysfunction and cognitive impairment in patient with chronic HE.