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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of hepatic encephalopathy has been investigated in a two-stage devascularization model in the rat with portavacal shunt and hepatic artery ligation. There is a significant increase in brain octopamine and phenylethanolamine and a decrease in brain norepinephrine (NE) 6 to 9 hours after hepatic artery ligation. The depletion of NE seems the sequel of diminished synthesis in the presence of an unaltered turnover rate, due to a blockade of tyrosine hydroxylase either by accumulation of false neurochemical transmitters or by phenylalanine. It is most marked in the cortex and midbrain. The high-energy phosphate compounds, ATP, phosphocreatine and glucose-6-phosphate are not diminished in hepatic coma, nor is glucose, indicating that other mechanism are involved in the pathogenesis of metabolic state by the increased ammonia level. "intestinal sterilization" and total colectomy have no significant effect on the ammonia level, but cause a decrease in the level or aromatic precursor amino acids in the plasma and brain, with normalization of the level of cerebral transmitters. These results permit the formulation of a unified concept of the hepatic coma syndrome and its clinical manifestations such as flapping tremor, the hyperdynamic cardiovascular state and the hepatorenal syndrome. Moreover, they form the basis for the introduction of a new therapeutic principle in the management of hepatic encephalopathy by L-dopa or modified amino acid solutions, which act by altering the central and peripheral neurotransmitters.
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PMID:[Cerebral manifestations in the hepatic coma syndrome (author's transl)]. 0 92

The dog with an end-to-side portacaval shunt (PCS) has been extensively used as a model to investigate hepatic encephalopathy (HE) as it demonstrates a plasma amino acid pattern similar to patients with chronic liver disease. In adult mongrel dogs, the effect of PCS on plasma and CSF amino acids, octopamine (OCT), phenylethanolamine (PEA) and CSF 5-hydroxyindolacetic acid (5-HIAA), were studied. Moreover, the effect of correction of plasma amino acids by infusional techniques was investigated.Tyrosine, tryptophan and phenylalanine levels increased dramatically during the development of HE in plasma and CSF, while valine, leucine and isoleucine decreased in plasma only, but CSF levels remained stable. Plasma and CSF octopamine and phenylethanolamine and CSF 5-HIAA increased markedly as clinical features in the dogs' behavior, characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence and finally coma. Once in coma, the dogs were infused with an amino acid mixture (F080) calculated to normalize the plasma amino acid pattern. After one to eight hours, the dogs began to awake. Simultaneously, blood, and CSF aromatic amino acids returned to their control values, as did OCT, PEA and CSF 5-HIAA. If F080 infusion was stopped, biochemical alterations would appear within one week, again accompanied by clinical hepatic encephalopathy.The results indicate that the altered levels of aromatic and branched chain amino acids, octopamine and PEA in plasma and CSF correlate well with the development of HE and that correction of the plasma amino acid abnormalities improves encephalopathy simultaneously with correction of neurotransmitter derangements in CSF.
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PMID:Alterations in plasma and CSF amino acids, amines and metabolites in hepatic coma. 63 94

A patient with cryptogenic cirrhosis was found to have corneal pigmentation rings indistinguishable from Kayser-Fleischer rings on slit-lamp examination. Although she had hepatic encephalopathy that included confusion, tremor, and slurred speech, diagnosis of Wilson's disease was ruled out because urinary cooper excretion and hepatic copper concentrations were below the range found in symptomatic Wilson's disease. The exact nature of these rings could not be determined, and they were considered as Kayser-Fleischer-like rings.
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PMID:Kayser-Fleischer-like ring in a cryptogenic cirrhosis. 71 54

The clinical syndrome of portal-systemic encephalopathy is caused by far advanced cirrhosis of the liver in most cases; it is characterized by increasing drowsiness, disturbances of mentation, flapping tremor and hyperreflexia. An early diagnosis can be established by testing writing and drawing abilities. Increased occurrence of spider nevi, a dry, deep red tongue, and hemorrhagic lesions of skin and mucous membranes are symptoms of incipient hepatic insufficiency. The syndrome is initiated in most cases by excessive intake of protein or alcohol, by intestinal bleeding, by diuretics, or by intercurrent infections. Therapy has to include elimination of causes, reduced intake of protein, enemas with acetate buffer solution and oral medication with lactulose, bifidum milk, and certain amino acids in order to lower hyperammoniemia; in serious cases neomycin has to be given. At the same time a normalization of fluid and electrolyte balance has to be achieved; replacement of potassium is especially important, when hypokalemia and alcalosis are present. In general prognosis of portal-systemic encephalopathy however is serious, depending primarily upon the fact, whether or not sufficient functional hepatic parenchyma is present.
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PMID:[Clinical picture and therapy of portal-systemic encephalopathy (author's transl)]. 89 27

A case of hepatic encephalopathy secondary to a large-caliber porto-hepatic venous shunt in a 61-year-old woman with gastric cancer is reported. Mild confusion, flapping tremor and hyperammonemia were noted preoperatively. Abdominal ultrasonography showed a large-caliber porto-hepatic venous shunt in the left lateral segment of the liver. Percutaneous transhepatic portography and superior mesenteric angiography were confirmatory. Intraoperative portal scintigraphy was performed before and after temporary shunt occlusion to measure the intrahepatic shunt rate, which decreased markedly after occlusion. Portal pressure was also measured, and increased only slightly after occlusion. Left lateral hepatic segmentectomy, and subtotal gastrectomy with splenectomy were performed. Hepatic encephalopathy resolved postoperatively. The shunt was thought to be acquired. The relevant reports on large-caliber porto-hepatic venous shunts in the literature are reviewed.
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PMID:Hepatic encephalopathy secondary to a large-caliber porto-hepatic venous shunt. A case report. 142 74

This case demonstrates focal neurologic deficit mimicking stroke with underlying hepatic encephalopathy. Unilateral weakness in patients with hepatic encephalopathy has not been previously described in the English language literature. A 46-yr-old white woman was admitted to an acute care hospital for left shoulder manipulation, underwent general anesthesia and appeared to have had a right cerebrovascular accident. At transfer to the rehabilitation hospital, in addition to the left hemiparesis, there were inconsistencies in the neurologic examination and signs of cognitive impairment and liver failure. The patient's response to an intensive, multidisciplinary inpatient rehabilitation program along with treatment of the liver dysfunction led to resolution of left-sided weakness and flapping tremor with independence in ambulation and activities of daily living. Relevant literature is reviewed. A thorough history and physical examination with liver function assessment should always be performed in patients with cerebrovascular accident and unusual recovery.
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PMID:Hepatic encephalopathy mimicking stroke. A case report. 155 31

A 53-year-old woman developed symptoms of slow speech, mild dementia, increased deep tendon reflex, ataxic gait, flapping tremor, and dystonic posture during two years. She had liver cirrhosis and hyperammonemia, which suggested a diagnosis of portal-systemic encephalopathy. MR T1-weighted images showed increased signal intensity in globus pallidus, internal capsule, substantia innominata, and a part of hypothalamus. T2-weighted images revealed abnormal findings as follows: high intense area in middle cerebellar peduncle, and low signal intensity of corpus callosum and pontine base. This is the first report about MRI abnormalities in substantia innominata, corpus callosum, and pontine base in a patient with portal-systemic encephalopathy.
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PMID:[A case of portal-systemic encephalopathy presenting characteristic MR images in globus pallidus, hypothalamus, corpus callosum, pontine base, and middle cerebellar peduncle]. 161 82

A 58-year-old male liver cirrhosis patient, who had a history of recurrent hepatic encephalopathy, was admitted to our hospital because of clouding of consciousness. He had an episode of recent head trauma. On admission, he was drowsy and exhibited flapping tremor, fetor hepaticus and ascites. Laboratory data showed an increase in blood ammonia level, and a decrease in peripheral thrombocytes, serum albumin and prothrombin value. A ratio of branched-chain to aromatic amino acids was reduced. Antibody against hepatitis C virus was positive. His electroencephalogram showed bilaterally large synchronous slow waves. He was treated with intravenous branched-chain amino acids, and recovered. Cranial computed tomography on day 9 demonstrated a crescent shaped area of low density in the right frontotempoparietal subdural region. He was diagnosed as chronic subdural hematoma, which was treated surgically. It has been suggested that chronic subdural hematomas develop as a complication of hemostatic deficiency due to liver cirrhosis.
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PMID:[A case of liver cirrhosis associated with chronic subdural hematoma and hepatic encephalopathy]. 174 68

A wide variety of movement disorders are associated with alcohol abuse. Some idiopathic movement disorders are markedly improved by small amounts of alcohol and this response occasionally may lead to alcoholism. Alcohol abuse alone or combined with hepatic encephalopathy can cause various types of tremor, asterixis, and cerebellar dysfunction. Alcohol withdrawal is occasionally complicated by transient basal ganglia dysfunction manifested by parkinsonism or chorea. These syndromes are distinct from the movement disorders complicating acquired hepatolenticular degeneration occurring in some chronic alcoholics. This review discusses the clinical and pathophysiologic aspects of the movement disorder syndromes that complicate alcohol abuse.
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PMID:Movement disorders in alcoholism: a review. 201 Dec 71

A case of a patient with severe liver dysfunction and hyperammonemia undergoing splenectomy and liver biopsy was reported. Preoperative examination revealed that this patient's liver function was severely impaired due to liver cirrhosis (ICG15 = 60%, HPT = 29%, serum NH3 = 110 micrograms.dl-1). Preoperatively, kanamycin 2 g.day-1 and lacturose 60 ml.day-1 were given and FFP 3-5 units.day-1 were infused. With no premedication, general anesthesia was induced with dTc 3 mg, thiopental 200 mg and SCC 80 mg. Anesthesia was maintained with N2O-O2-enflurane and pancuronium. Though N2O concentration was kept at 50% to prevent intraoperative hypoxemia, the necessary enflurane concentration was low (almost 1% or lower). Serum NH3 level during operation was stable (100-110 micrograms.dl-1), and the level decreased (66-90 micrograms.dl-1) postoperatively. Postoperatively, this patient's consciousness level fluctuated with or without flapping tremor. The treatment of hepatic encephalopathy with lactulose, aminoleban EN and maalox were effective. Problems of perioperative and anesthetic management of a patient for upper abdominal surgery with severe liver dysfunction associated with hyperammonemia were discussed.
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PMID:[Anesthetic experience of a patient for splenectomy with severe liver dysfunction and hyperammonemia]. 223 30


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