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
ABSTRACT 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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ABSTRACT: The term hepatic encephalopathy (HE) covers a wide spectrum of neuropsychiatric abnormalities caused by portal-systemic shunting. The diagnosis requires demonstration of liver dysfunction or portal-systemic shunts and exclusion of other neurologic disorders. Most patients with this condition have liver dysfunction caused by cirrhosis, but it also occurs in patients with acute liver failure and less commonly, in patients with portal-systemic shunts that are not associated with hepatocellular disease. Various magnetic resonance (MR) techniques have improved our knowledge about the pathophysiology of HE. Proton MR spectroscopy and T1-weighted imaging can detect and quantify accumulations of brain products that are normally metabolized or eliminated such as glutamine and manganese. Other MR techniques such as T2-weighted and diffusion-weighted imaging can identify white matter abnormalities resulting from disturbances in cell volume homeostasis secondary to brain hyperammonemia. Partial or complete recovery of these abnormalities has been observed with normalization of liver function or after successful liver transplantation. MR studies have undoubtedly improved our understanding of the mechanisms involved in the pathogenesis of HE, and some findings can be considered biomarkers for monitoring the effects of therapeutic measures focused on correcting this condition.04/2014; 35(2):136-52. DOI:10.1053/j.sult.2013.09.008
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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.PLoS ONE 11/2012; 7(11):e48886. DOI:10.1371/journal.pone.0048886 · 3.53 Impact FactorThis article is viewable in ResearchGate's enriched formatRG Format enables you to read in context with side-by-side figures, citations, and feedback from experts in your field.
Article: Hepatische Enzephalopathie[Show abstract] [Hide abstract]
ABSTRACT: Die hepatische Enzephalopathie (HE) ist durch einen psychomotorischen Symptomenkomplex gekennzeichnet, welcher sich definitionsgem im Rahmen einer akuten oder chronischen Leberinsuffizienz entwickelt und in seltenen Fllen durch einen portokavalen Shunt ohne apparente Lebererkrankung ausgelst werden kann. Verursacht wird die HE durch aus dem Darm resorbierte oder im Rahmen des Metabolismus anfallende Substanzen, die normalerweise in der Leber einem First-Pass-Effekt unterliegen, bei Vorliegen einer eingeschrnkten hepatischen Eliminationsleistung bzw. portovenser Kollateralen jedoch nicht ausreichend entgiftet werden. Eine zentrale Position in der Pathogenese scheint Ammoniak einzunehmen, dessen zerebrale Wirkung noch nicht in allen Details bekannt ist. Die aktuellen pathogenetischen Hypothesen sind ein Gegenstand dieser bersicht. In Abhngigkeit von der Akuitt des zugrunde liegenden Leberversagens wird die HE in eine akute und eine chronische Form unterteilt. Die weitaus hufigere chronische HE kann persistierend oder episodisch auftreten, der letzteren Form liegen dann in der Regel bestimmte przipitierende Faktoren (z. B. Ditfehler, Infektion, gastrointestinale Blutung etc.) zugrunde. Das klinische Bild gliedert sich in fnf Stadien, die sich vor allem an der psychomotorischen Symptomatik und der zunehmenden Komatiefe orientieren. In der Diagnostik steht nach Ausschluss anderer Komaformen die klinische Beurteilung im Vordergrund. Bei der Einleitung therapeutischer Manahmen muss bei allen Formen der HE die Lebertransplantation als kausale Therapieoption geprft werden, zumal diese im Rahmen eines akuten Leberversagens durch die Mglichkeit der high urgency-(HU-)Meldung kurzfristig zur Verfgung steht. Die symptomatische Therapie vor allem der chronischen HE hat drei prinzipielle Ziele: 1. Allgemeinmanahmen wie Sicherung einer adquaten Oxygenierung, Regulation des Blutzuckerspiegels und ausreichende Ernhrung; 2. Identifizierung des przipitierenden Faktors und dessen Beseitigung, wobei der bergang von der Akuttherapie zur Prophylaxe bei der chronischen HE flieend ist; 3. Reduktion ammoniagener Substrate im Darm und in der Zirkulation. Diese Behandlungsziele werden bei der akuten HE durch eine effektive Prophylaxe bzw. Therapie des drohenden Hirndems ergnzt.Hepatic encephalopathy (HE) may develop within the course of acute or chronic liver failure and is characterized by a complex of psychomotor symptoms. In addition, HE can be induced by portocaval shunting even in the absence of any apparent liver disease. HE is caused by substances, which are either reabsorbed from the gut or are a product of the body metabolism. Normally, these substances are effectively eliminated during their first passage through the liver. However, a decreasing number of functional hepatocytes or the presence of portocaval collaterals in liver disease may significantly impair hepatic detoxification. Ammonia seems to take a central position in the pathogenesis of HE, although the exact cerebral effects of this metabolite are still not known in detail. The actual pathogenetic hypotheses are subject of this review. Depending on the underlying liver disease, HE is divided into an acute and a chronic form. Chronic HE may be present as a persistent or an episodic form, the latter being usually induced by defined precipitating factors, such as diet failures, infection and gastrointestinal-bleeding. With regard to the psychomotor symptoms and the coma depth, the clinical picture is classified into five grades (West Haven criteria). Diagnosis is made by clinical examination of the mental status after relevant differential diagnoses have been excluded. The only causal therapeutic option in the presence of acute or chronic liver failure is liver transplantation. Therefore, the indication for transplantation has to be evaluated in all forms of HE. Symptomatic treatment has three principal aims: (1) stabilization of circulation, oxygen supply, blood sugar and nutrition; (2) identification of the precipitating factor and its removal; (3) reduction of ammonia and other potential toxins in the circulation. In the case of acute HE, these therapeutic aims are complemented by an effective prophylaxis or therapy of brain edema.09/2004; 99(10):591-602. DOI:10.1007/s00063-004-1090-x