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.
Article: Hepatische Enzephalopathie[Show abstract] [Hide abstract]
ABSTRACT: Die hepatische Enzephalopathie (HE) ist eine neuropsychiatrische Komplikation akuter und chronischer Lebererkrankungen. Ursache ist eine komplexe, metabolisch induzierte und damit potenziell reversible Funktionsstrung des Gehirns. Voraussetzung fr die Diagnose einer HE ist der Nachweis einer Funktionsstrung des zentralen Nervensystems bei gleichzeitig bestehender Leberfunktionsstrung und sicherem Ausschluss einer neurologischen oder psychiatrischen Erkrankung anderer tiologie. Die Diagnose einer HE wird rein klinisch gestellt und umfasst ein weites Spektrum neuropsychiatrischer Symptome unterschiedlicher Schweregrade. Die ergnzende Zusatzdiagnostik beinhaltet labormedizinische Methoden, bildgebende Verfahren und neurophysiologische Zusatzuntersuchungen. Die Therapie der HE besteht im Wesentlichen aus der Behandlung und zuknftigen Vermeidung auslsender Faktoren, der Modulation metabolischer Prozesse sowie ultima ratio der Lebertransplantation. Die Prognose hngt von der Art und dem Verlauf der hepatischen Grunderkrankung ab.Hepatic encephalopathy (HE) is a neuropsychiatric complication of acute and chronic liver disease. Its etiology and pathogenesis are thought to be a complex, metabolically induced, and therefore potentially reversible disturbance in brain functions. The diagnosis is based on demonstrating both a disorder of the central nervous system and a concomitant liver disease as well as the exclusion of any neurological or psychiatric disorder of other etiology. The diagnosis of HE is clinical and displays a wide spectrum of neuropsychiatric symptoms in different degrees of severity. Ancillary diagnostic workup includes laboratory tests, neuroimaging, and neurophysiological exams such as electroencephalography and evoked potentials. The therapy of HE mainly consists of treatment and avoidance of any precipitating conditions such as high protein intake, infections, and gastrointestinal bleeding. Other therapeutic approaches modulate metabolic processes such as ammonium synthesis and excretion, formation of neurotransmitters, and as a last resort liver transplantation. The prognosis depends ultimately on the course of the liver disease.Der Nervenarzt 11/2003; 74(12):1078-1087. · 0.80 Impact Factor
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ABSTRACT: The purpose of this study was to evaluate the clinical features and the characteristics of MR images of patients with end-stage hepatic failure. We reviewed the MR findings and clinical features of 31 consecutive patients (20 men, 11 women=31, mean age 58.7 years) who had been diagnosed with clinical hepatic encephalopathy. Associations between the lesion locations on each MR sequence were analyzed using a binominal test. The clinical and MR findings were compared in relation to the etiology and clinical status. The most frequently involved site, seen as high signal intensity on T2-W images, was the corpus callosum (20 patients), followed by the dentate nucleus (16 patients) and the globus pallidus (13 patients). Significant associations were seen between the pallidus and the crus cerebri, between the crus cerebri and the red nucleus, between the crus cerebri and the dentate nucleus, and between the red nucleus and the dentate nucleus on the T2-W and DW images (P < 0.004). The crus cerebri, red nucleus, and dentate nucleus were involved concurrently with the corpus callosum more frequently in hepatic encephalopathy grades 3 and 4. Concurrent involvement of the globus pallidus-crus cerebri-red nucleus-dentate nucleus axis was the main MR pattern in end-stage hepatic encephalopathy, which connected with various areas of the brain. We hypothesize that these overlapping MR features could be regarded as an entity denoted as the "hepatic encephalopathy continuum".Neuroradiology 05/2008; 50(8):683-91. · 2.70 Impact Factor
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ABSTRACT: Hyperammonemic encephalopathy is a type of metabolic encephalopathy with diversified etiology. Hyperammonemia is the end result of several metabolic disorders such as congenital deficiencies of urea cycle enzymes, hepatic encephalopathy, Reye's syndrome and other toxic encephalopathies. Non-specific clinical presentation poses a great challenge in early diagnosis of this entity. Irrespective of the underlying etiology, hyperammonemia causes a distinctive pattern of brain parenchymal injury. The cingulate gyrus and insular cortex are more vulnerable to this type of toxic insult. Characteristic magnetic resonance imaging findings in combination with laboratory parameters can help to differentiate this entity from other metabolic encephalopathy and thus aiding in early diagnosis and treatment.Acta neurologica Belgica 02/2012; 112(2):221-3. · 0.47 Impact Factor