Department of Neurology, Faculty of Medicine, P. J. Safárik University, Tr. SNP 1, 040 66 Koice, Slovak Republic
Received 21 August 2000; in revised form 9 February 2001; accepted 21 February 2001
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ABSTRACT |
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INTRODUCTION |
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Transcranial Doppler sonography (TCD) is a non-invasive method which can measure cerebral blood flow velocity. That is why we have decided to use this method to study blood flow velocity in heavy alcohol drinkers, to see if there are changes, as in patients with stroke.
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MATERIALS AND METHODS |
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The middle cerebral artery (MCA) mean flow velocity (Vmean) was determined by a 2 MHz pulsed Doppler probe (Trans-scan 3-D; EME, Germany) maintained in the temporal area by a headband with insonation through the middle temporal window at a depth of 5055 mm during the first 2 days after admission to hospital. The pulsatility index [PI = (VsVd): Vmean] was also determined.
Extracranial carotid arteries were examined by Doppler sonography and there was no evidence of internal or common carotid artery stenosis.
The results were compared with the blood flow velocity in the middle cerebral artery in 20 healthy volunteers (all men) of the same age with similar smoking habits. A total of 29% of the patients and 30% of the controls were non-smokers. To obtain detailed information about smoking habits in heavy alcohol drinkers is very difficult. Differences between these two groups were tested with Student's t-test. P < 0.01 was selected as the point of minimal statistical significance.
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RESULTS |
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DISCUSSION |
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Reduced cerebral blood flow measured by single photon emission computed tomography in subjects with liver cirrhosis was observed by Melgaard et al. (1990) and Iwasa et al. (2000).
A statistically significant decrease in blood flow in the middle cerebral artery has been described by Dillon et al. (1995) in patients with cirrhosis without clinically apparent encephalopathy, as well as by Larsen et al. (1995) who explained it on the basis of impaired autoregulation of cerebral blood flow.
Delirium, changes in behaviour or decision to stop drinking, but not liver problems, were the reasons for admission to the hospital. This is why liver biopsy was not performed, and, consequently, no classification of liver disease was made.
Strauss et al. (2000) described impaired autoregulation only in patients with hepatic encephalopathy and not in all patients with end-stage liver disease. Restoration of cerebral blood flow autoregulation was shown within 48 (24120) h after spontaneous hepatic recovery or liver transplantation, but before complete alleviation of hepatic encephalopathy (Strauss et al., 1997). The authors did not consider impaired autoregulation to be of major pathophysiological importance in hepatic encephalopathy.
The aim of our study was to determine if heavy alcohol drinking influences cerebral blood flow velocity with regard to the possibility of association between alcohol abuse and ischaemic brain infarction. Low blood flow velocity in cerebral arteries which could be a risk factor for stroke was found. A liver lesion may be one of the reasons for impaired circulation. Differences in blood flow velocity in our patients were not dependent on psychological changes. Other factors must therefore be involved.
One such factor could be increased blood viscosity. Decreased blood flow velocity in patients with increased blood viscosity was described by Dormandy (Dormandy, 1983). Significant elevation of viscosity of both whole blood and plasma before stroke has been reported by Coull et al. (1991) and a significant decrease in erythrocyte deformability was observed on the first day after stroke (Moj
i
et al., 1999
).
However, it is still unclear what causes decreased blood flow velocity. Blood and plasma viscosity, erythrocyte deformability and dehydration could be potential determinants and thus merit investigation.
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ACKNOWLEDGEMENTS |
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REFERENCES |
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