MR imaging and spectroscopy of the basal ganglia in chronic liver disease: Correlation of T1-weighted contrast measurements with abnormalities in proton and phosphorus-31 MR spectra
The purpose of this study was to correlate the hyperintensity in the globus pallidus seen on T1-weighted magnetic resonance imaging (MRI) of the brain in chronic liver disease with changes in metabolite ratios measured from both proton and phosphorus-31 magnetic resonance spectroscopy (MRS) localised to the basal ganglia. T1-weighted spin echo (T1 WSE) images were obtained in 21 patients with biopsy-proven cirrhosis (nine Child's grade A, eight Child's grade B and four Child's grade C). Four subjects showed no evidence of neuropsychiatric impairment on clinical, psychometric and electrophysiological testing, four showed evidence of subclinical hepatic encephalopathy and 13 had overt hepatic encephalopathy. Signal intensities of the globus pallidus and adjacent brain parenchyma were measured and contrast calculated, which correlated with the severity of the underlying liver disease, when graded according to the Pugh's score (p<0.05). Proton MRS of the basal ganglia was performed in 12 patients and 14 healthy volunteers. Peak area ratios of choline (Cho), glutamine and glutamate (Glx) and N-acetylaspartate relative to creatine (Cr) were measured. Significant reductions in mean Cho/Cr and elevations in mean Glx/Cr ratios were observed in the patient population. Phosphorus-31 MRS of the basal ganglia was performed in the remaining nine patients and in 15 healthy volunteers. Peak area ratios of phosphomonoesters (PME), inorganic phosphate, phosphodiesters (PDE) and phosphocreatine relative to BATP (ATP) were then measured. Mean values of PME/ATP and PDE/ATP were significantly lower in the patient population. No correlation was found between the T1WSE MRI contrast measurements of the globus pallidus and the abnormalities in the metabolite ratios measured from either proton or phosphorus-31 MR spectra. Our results suggest that pallidal hyperintensity seen on T1WSE MR imaging of patients with chronic liver disease is not related to the functional abnormalities of the brain observed in hepatic encephalopathy.
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- "However, we did not find a correlation between the GP signal intensity and abnormal corticostriatal functional connectivity or neuropsychiatric performances, although the cirrhotic patients had significantly higher signal intensity at the bilateral GP than healthy controls. This result was consistent with a previous finding demonstrating that there was no significant correlation between the GP hyperintensity and neuropsychiatric impairments  or metabolic disorders . This lack of correlation may be due to the indirect measurements, in which the hyperintensity on T1-weighted images represents abnormal manganese deposition . "
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ABSTRACT: Neurobiological and neuroimaging studies have emphasized the structural and functional alterations in the striatum of cirrhotic patients, but alterations in the functional connections between the striatum and other brain regions have not yet been explored. Of note, manganese accumulation in the nervous system, frequently reflected by hyperintensity at the bilateral globus pallidus (GP) on T1-weighted imaging, has been considered a factor affecting the striatal and cortical functions in hepatic decompensation. We employed resting-state functional magnetic resonance imaging to analyze the temporal correlation between the striatum and the remaining brain regions using seed-based correlation analyses. The two-sample t-test was conducted to detect the differences in corticostriatal connectivity between 44 cirrhotic patients with hyperintensity at the bilateral GP and 20 healthy controls. Decreased connectivity of the caudate was detected in the anterior/middle cingulate gyrus, and increased connectivity of the caudate was found in the left motor cortex. A reduction in functional connectivity was found between the putamen and several regions, including the anterior cingulate gyrus, right insular lobe, inferior frontal gyrus, left parahippocampal gyrus, and anterior lobe of the right cerebellum; increased connectivity was detected between the putamen and right middle temporal gyrus. There were significant correlations between the corticostriatal connectivity and neuropsychological performances in the patient group, but not between the striatal connectivity and GP signal intensity. These alterations in the corticostriatal functional connectivity suggested the abnormalities in the intrinsic brain functional organiztion among the cirrhotic patients with manganese deposition, and may be associated with development of metabolic encephalopathy. The manganese deposition in nervous system, however, can not be an independent factor predicting the resting-state brain dysfunction in real time.
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ABSTRACT: In vivo cerebral MRS techniques provide a non-invasive means of studying high energy phosphates levels and metabolites such as glutamine, glutamate and myoinositol in patients with CHE. Although there are differences in the 31P MRS findings between published studies, these are largely methodological, owing to variations in data acquisition with results on differing areas of the brain in small, but widely different patient populations. In order to obviate these discrepancies, future studies should concentrate on localised information from specific areas of the brain in clinically well-characterised groups of patients. There is greater concordance with proton MRS studies, all of which show an increased glutamine/glutamate resonance with increasing severity of CHE. MRS may be used to gain insight into the pathogenesis of the condition. Furthermore, since both 31P and proton MRS abnormalities correlate with neuropsychiatric status, the technique may afford the possibility of an objective and dynamic means of patient monitoring. MRS may also be of use in assessing the effectiveness of various treatment regimens.
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ABSTRACT: Neuropsychiatric abnormalities affecting patients with chronic liver disease are termed chronic hepatic encephalopathy. They involve neurotransmitter changes, rather than a structural disorder of the brain. Diagnosis is based on clinical findings, and electroencephalographic and psychometric testing. There is no 'specific' treatment, but there are a number of non-specific measures that can be used.
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