Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropsychological testing was performed on: 10 right-handed patients who had had 1-4 right hemisphere transient ischaemic attacks (TIAs), 10 normal controls, 10 house painters with long-term exposure to organic solvents, and 10 patients with liver cirrhosis. The subjects in each group were matched for age and education. No TIA patient had significant internal carotid artery stenosis, and CT was normal except in one patient, although magnetic resonance imaging (MRI) performed 3 years after the testing was abnormal in 4/8 cases. No patient reported additional distinct TIAs during the period between neuropsychological testing and MRI. The TIA patients showed lateralized signs of spatial impairment, whereas the cirrhotics and also (but to a lesser degree) the house painters showed signs of diffuse cerebral dysfunction. The study shows that hemispheric TIAs in patients without significant internal carotid artery stenosis may result in persistent focal cognitive impairment. This can be demonstrated with sensitive neuropsychological instruments even when MRI is normal.
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PMID:Spatial impairment following right hemisphere transient ischaemic attacks in patients without carotid artery stenosis. 258 7

Three hundred eighty-three alcoholics, who had at least once been ordered supervision or compulsory treatment at an institution for alcoholics by the Temperance Board, were compared with 383 other alcoholics matched for age and sex. All the alcoholics were first admitted to the Department of Psychiatry, University Hospital, Lund, during the years 1949 to 1969 and followed up until January 1, 1981. They were systematically rated concerning symptoms and etiological factors at first admission. According to a stepwise logistic regression analysis, the following initial symptoms were positively associated with later compulsory treatment: slight cerebral dysfunction/personality change, antisociality/criminality, and impaired social and work performance. Social pressure/responsibility/conflict, slight depression, and continuous drinking were positively associated with the controls. There were 168 deaths in the compulsory treatment group and 124 in the control group (p less than 0.01). The excess deaths in the compulsory treatment group were mainly caused by accidents, poisoning, and violence (21 cases) and sudden cardiac death (10 cases), while there were no differences concerning alcohol-related neoplasms and liver cirrhosis. The compulsory treatment group had a worse long-term social adjustment. The findings indicate that compulsory treatment was related to behavioral patterns showing a stability over time, supporting the validity of subclassification of alcoholics using social data.
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PMID:Alcoholics committed to treatment: a prospective long-term study of behavioral characteristics, mortality, and social adjustment. 327 54

Subjects with three different types of hepatic cirrhosis were compared on a battery of neuropsychological tests to determine if cerebral dysfunction varied according to the type of liver disease. It was found that the manifest cognitive impairments varied according to the type and etiology of the liver disease. These findings underscore the sensitivity of neuropsychological tests in the detection of hepatic encephalopathy, particularly in cases where there are no overt clinical signs or symptoms of neurologic disturbance. They also suggest that the nature and severity of the measurable neuropsychological abnormalities may vary within patient populations depending upon the etiology of the individual's liver disease and the specific pathophysiological mechanisms involved in its progression.
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PMID:Neurobehavioral correlates of cholestatic and hepatocellular disease: differentiation according to disease specific characteristics and severity of the identified cerebral dysfunction. 359 34

Acutely increased intraabdominal pressure can lead to multisystem organ dysfunction. Organ dysfunction consists of acute pulmonary failure secondary to compressive atelectasis and associated with high peak inspiratory pressures and impaired gas exchange, acute renal failure with marked oliguria without hypernaturia, intestinal and hepatic ischemia possibly leading to bacterial translocation or necrosis with peritonitis, increased intracranial pressures which may cause brain dysfunction or aggravate head injury edema, venous thrombosis and thromboembolism, and abdominal wall ischemia or necrosis. The diagnosis is made clinically in a patient with high peak inspiratory pressures, oliguria and an apparently tight abdomen, although urinary bladder pressure > or = 20 cm H2O pressure is suggestive. However, chronically increased intraabdominal pressure as is seen in the morbidly obese, pregnancy and cirrhosis may be misleading. As to treatment, once the diagnosis is made, the patient's abdomen should be opened and the tension relieved. The intestinal contents need to be protected and evaporative water loss minimized by either closing the skin and not the fascia or, if this is not possible, using an impermeable protective dressing. If the abdomen is difficult to close at the primary operation, it is best to prevent the development of an acute abdominal compartment syndrome by closing only the skin or leaving it open and using an impermeable dressing. In conclusion, the acute abdominal compartment syndrome has become increasingly recognized as a cause for multisystem organ failure. Recognition of the problem or prevention is mandatory for optimal patient survival.
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PMID:Multisystem organ failure secondary to increased intraabdominal pressure. 1144 Mar 93

The alcohol-withdrawal syndrome is a well-known clinical situation, so does its treatment. However, new researches have shown that the risk of severe withdrawal manifestations increases proportionally with the number of previous detoxifications, according to a sensitisation stress model. As a consequence, special attention should be paid to patients with a clinical history of multiple alcohol detoxifications, even if they never previously had delirium tremens and/or comitiality. Even in the absence of characteristic neurologic lesions, long-lasting heavy drinking is associated with brain dysfunction, concerning mostly the frontal cortex. This is clinically associated to neuropsychological deficits, specifically disorders of working memory and the so-called "executive functions". These deficits have a dramatic importance, because they impair drastically the outcome of alcoholic patients after detoxification. In Belgium like in other countries, an increasing prevalence of hepatitis C is present in alcoholic patients. This is due probably to the increase of a former illegal drugs consumption in those patients. This association between alcoholism and hepatitis C is of major importance, because alcohol consumption increases the viral load and the risk of cirrhosis and hepatocarcinoma. Furthermore, alcohol reduces the response to interferon therapy.
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PMID:[Clinical and therapeutic aspects in the treatment of alcohol addiction]. 1242 55

This study assessed cognitive deficit in patients diagnosed with different stages of hepatic cirrhosis and in liver transplant recipients. A short protocol consisting of several psychometric tests was used. Cirrhotic patients showed a degree of mental impairment in all the functions studied. The severity of the deficit was related to the degree of hepatic dysfunction. In contrast, liver transplant recipients presented only a slightly altered cerebral dysfunction in comparison to the control group. Their cognitive capacity was slightly better than that of patients with asymptomatic cirrhosis.
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PMID:Cognitive deficits in patients with hepatic cirrhosis and in liver transplant recipients. 1255 77

Hepatic encephalopathy is the most obvious neurological consequence of chronic hepatitis C virus (HCV) infection. There are also case reports of HCV-associated cerebral vasculitis. This review is concerned with the possibility of an effect of HCV on cerebral dysfunction, occurring at an early stage of chronic infection, prior to the development of cirrhosis and unrelated to vasculitis. There is emerging evidence of mild, but significant neurocognitive impairment in HCV infection, which cannot be attributed to substance abuse, coexistent depression, or hepatic encephalopathy. In vivo magnetic resonance spectroscopy and neurophysiological studies have suggested that a biological mechanism may underlie these cognitive findings. The recent detection of HCV genetic sequences in postmortem brain tissue raises the intriguing possibility that HCV infection of the central nervous system may be related to the reported neuropsychological symptoms and cognitive impairment.
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PMID:Central nervous system involvement in hepatitis C virus infection. 1555 29

Minimal hepatic encephalopathy (MHE) is frequently diagnosed in patients with liver cirrhosis who do not show overt clinical cirrhosis-associated neurological deficits. This condition manifests primarily with visuo-motor and attention deficits. We studied the association between visuo-motor deficits and magnetic resonance spectroscopic parameters in cingulate grey matter and white matter of centrum semiovale in patients with liver cirrhosis. The data revealed an increase in the glutamate-glutamine/creatine ratio and a decrease in choline/creatine and inositol/creatine ratios in patients with liver cirrhosis. The analysis of the data showed that cirrhosis-associated deterioration of the visuo-motor function significantly correlates with a decrease in the choline/creatine ratio and an increase in N-acetylaspartate/choline in cingulate grey matter but not in the neighbouring white matter. Furthermore, the increase in the glutamate-glutamine/creatine ratio correlated significantly with the increase in the N-acetylaspartate/creatine ratio. These data suggest an association between altered choline, glutamate-glutamine and NAA metabolism in cingulate grey matter and symptoms of MHE, and underline the importance of differentiation between grey and white matter in magnetic resonance spectroscopic studies on patients with cirrhosis-associated brain dysfunction.
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PMID:Chemical shift magnetic resonance spectroscopy of cingulate grey matter in patients with minimal hepatic encephalopathy. 1565 60

The clinical presentation of acute liver failure and hepatic encephalopathy (HE) in patients with cirrhosis differs significantly. The most serious neurological complication of acute liver failure is the development of devastating brain oedema. Therefore, intracranial pressure monitoring is urgently needed in these patients. Brain oedema is amplified by hypoglycemia, hypoxia and seizures, which are also frequent complications of acute liver failure. Therefore, these parameters must also be monitored. In contrast to acute liver failure in which cerebral dysfunction progresses rapidly, cognitive decline may be clinically undetectable for a long time in cirrhotic patients, until clinically overt symptoms such as psychomotor slowing, disorientation, confusion, extrapyramidal and cerebellar symptoms or a decrease in consciousness occur. Clinically, overt HE is preceded by minimal alterations of cerebral function that can only be detected by neuropsychological or neurophysiological measures, but which nevertheless interfere with the patient's daily living. Rapidly progressing spastic paraparesis (hepatic myelopathy) is a rare complication of cirrhosis. In contrast to HE, it does not respond to blood ammonia lowering therapies but must be considered as an indication for urgent liver transplantation. Cognitive dysfunction has recently been detected in hepatitis C virus (HCV)-infected patients with normal liver function. The patients presented with severe fatigue, cognitive dysfunction and mood disorders. Alterations in brain metabolites, as detected by magnetic resonance spectroscopy, indicated central nervous system alteration in these patients. In contrast to patients with HE, HCV-infected patients did not show motor symptoms or deficits in visual perception, but considerable deficits in attention and concentration ability.
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PMID:Neurological and neuropsychiatric syndromes associated with liver disease. 1625 35

Patients with chronic hepatitis C virus (HCV) infection frequently describe neuropsychological symptoms. Although hepatic encephalopathy is the best established neurological association of HCV infection, there is a growing body of literature on cerebral dysfunction, occurring at an early stage of chronic HCV infection, well before the development of cirrhosis. In this review we describe recent studies that have documented mild, but significant neurocognitive impairment in HCV infection. These deficits in patients with minimal or absent liver disease do not appear to be attributable to a history of substance abuse, coexistent depression or hepatic encephalopathy. Recent studies employing in-vivo magnetic resonance spectroscopy have suggested that a biological mechanism associated with the virus may be responsible. The hypothesis that HCV infection of the central nervous system may be related to the reported neuropsychological symptoms and cognitive impairment is supported by molecular virological studies of post-mortem brain tissue.
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PMID:Central nervous system changes in hepatitis C virus infection. 1653 3


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