Gene/Protein Disease Symptom Drug Enzyme Compound
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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

Ten new cases of perhexiline induced peripheral neuropathies are reported. The authors emphasize the possible association of other neurological disorders: cerebellar symptoms in one case, complex tremor in two other cases, marked decrease of photomotor reflexes in one case and disgeusia in another one. The pharmacocinetic study of 4 cases revealed the presence of a low metabolism of the drug in one of them. Polymorphous inclusions have been seen in Schwann cell and endothelial cell cytoplasm in the three patients with electron microscopic study of the nerves. The pathological study of one case showed the demyelination of spinal cord posterior columns. In another case, who died from hepatic coma, the biochemical study of cerebral lipids revealed the low values of cerebrosides and sulfatides in cerebellum and cerebral white matter.
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PMID:[Neurological disorders and perhexiline maleate therapy. Clinical study of 10 cases. Neuropathological, pharmacocinetic and biochemical studies (author's transl)]. 21 69

So as to assess the effects of lithium carbonate on peripheral leucocyte levels of hepatic cirrhosis patients, 10 cirrhotic patients were studied with less than 4,500 leukocytes per cubic ml and without contraindications for lithium salts that were administered for three weeks at a dose of 90 mg daily. At the end of each week total peripheral leukocytes, differential formula, platelet count and serum lithium concentration determinations were made. In the basal stage, total leukocyte average was 3,400 +/- 527 (X +/- DE) and granulocyte average was 2,090 +/- 341. After the first week of lithium treatment a significant increase was observed in total leukocyte and granulocyte levels whose averages at the end of the third week of treatment were 4,800 +/- 1,052 (p less than 0.01) and 3,694 +/- 1,003 (p less than 0.001) respectively. There was no correlation between the magnitude of leukocyte increase and serum lithium levels obtained that ranged from 0.28 and 1.32 mEq/l. Three patients showed transient gross tremor and two suffered hepatic coma. We can conclude that lithium carbonate increases peripheral leucocytes at the expense of neutrophilia in patients with secondary granulocytopenia and hypersplenism resulting in liver cirrhosis.
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PMID:Effects of lithium carbonate on leucocytes of hepatic cirrhosis patients. 679 6

Hepatic encephalopathy (HE) is clinically characterized by a large variety of symptoms including motor symptoms, cognitive deficits, as well as changes in the level of alertness up to hepatic coma. A number of pathological processes affecting glial and neuronal function have been identified, including hyper-ammonia, changes within the excitatory and inhibitory transmitter systems, as well as osmolytic changes with consecutive cell swelling. One explanation how these pathological processes result in neurological deficits in HE is the concept of pathologically synchronized oscillations within and between relevant brain regions. A number of studies suggest that the cognitive deficits and the reduced level of alertness in patients with HE can be attributed to a significantly slowed and pathologically synchronized spontaneous oscillatory brain activity, depending on the grade of HE. Moreover, HE motor symptoms, like postural tremor called"mini asterixis," have recently been shown to be associated with abnormal thalamo-cortical and cortico-muscular synchronization. Indirect evidence exists from studies of processing and recognition of flicker stimuli that in HE slowing of oscillations also occurs in the visual system. Taken together, pathological synchronization of neuronal activity may turn out to be a promising pathophysiological concept for linking neuronal dysfunction to the diversity of clinical deficits in HE.
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PMID:Neural synchronization in hepatic encephalopathy. 1638 44