[Brain damage associated with alcoholism].
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Alcohol Amnestic Disorder↗
Biomedical subjects
M Hillbom
Publications and source records attributed to M Hillbom.
Does alcohol intoxication precipitate aneurysmal subarachnoid haemorrhage?
Seventy-five consecutive patients aged 15 to 55 years with aneurysmal subarachnoid haemorrhage verified by CSF examination and cerebral angiography or at necropsy were studied. In 19 cases (25%; four women and 15 men) the bleeding was preceded within 24 hours by a bout of alcohol drinking. Alcohol-related cases composed 33% and 14% of the patients in the age groups 15-40 and 41-55 years, respectively. Alcohol intoxication preceding the subarachnoid haemorrhage was two to four times as common in male and three to five times as common in female patients as alcohol intoxication in the general Finnish population of the same age and sex. Occasional alcohol intoxication seems to carry an increased risk of aneurysmal subarachnoid haemorrhage.
Adolescent↗
Creatine kinase isoenzymes in acute brain injury.
Brain-type creatine kinase (CK) isoenzyme (CK-BB) was detected in the serum in 13 out of 26 patients with acute brain injury (50%). The peak of CK-BB activity ranged from 5 to 188 U/liter, constituting, on average, 10.5% of the total CK activity. The highest activities were seen in patients with gunshot wounds. High CK-BB activity was associated with poor prognosis, but minimal CK-BB elevations did not have prognostic significance. Heart-type creatine kinase isoenzyme (CK-MB) was detected in the serum in 17 out of 26 patients (65%). The peak activity ranged from 5 to 115 U/liter, constituting, on average, 6.6% of total CK activity. Electrocardiogram taken from 20 patients revealed transient T-wave inversions in the precordial leads in four patients; three of them also showed serum CK-MB activity. Subendocardial hemorrhage was detected at autopsy in three of the five CK-MB-positive patients, but in none of the four CK-MB-negative cases. Present findings suggest that acute brain injury may be secondarily cause myocardial damage.
Adolescent↗
[Neurosyphilis].
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Diagnosis, Differential↗
Low acetaldehyde levels in blood, breath and cerebrospinal fluid of intoxicated humans as assayed by improved methods.
A sensitive method for determination of human blood acetaldehyde (AcH), which avoids artefactual ethanol-derived Ach formation, was developed. AcH was trapped by collecting blood directly into isotonic semicarbazide, the plasma separated, AcH liberated by perchloric acid and analyzed by gas chromatography. Breath AcH was also trapped in semicarbazide and analyzed similarly. Using an experimentally determined blood:breath partition ratio of 190, calculated pulmonary blood and measured antecubital blood AcH were very similar at various concentrations. Blood AcH was found generally to be very low (< 10 microM) at moderate ethanol levels. Calcium carbimide (0.25 mg/kg) caused moderate flushing reactions and elevated AcH to 25-188 microM. 4-Methylpyrazole (5 mg/kg i.v.) rapidly attenuated AcH levels and symptoms, indicating its potential use in the treatment of disulfiram-ethanol reactions. AcH in the cerebrospinal fluid of 5 highly intoxicated patients was almost absent (0-5 microM). Blood AcH in occasional or chronic alcohol abusers were generally low (< 10 microM), elevated AcH levels being observed only in association with clinical abnormalities. The results indicate that in general, previously reported human blood AcH levels are erroneously high and that breath levels reflect blood levels. Blood AcH may play a lesser role in the actions of ethanol in humans than is often assumed.
Acetaldehyde↗
Peripheral neuropathy and myopathy. An experimental study of rats on alcohol and variable dietary thiamine.
The effects of variable dietary thiamine concentrations (deficient, normal, surplus) on the development of alcoholic neuromyopathy in rats exposed for 36 weeks to 10-25% (v/v) ethanol or water (control group) as the sole drinking fluid were studied by histological and electrophysiological methods. Abnormalities in the structure of the sciatic nerve (phagocytosis, myelin abnormalities, increase in nonspecific cholinesterase activity) and tibial muscles (angular atrophic fibers, group atrophy, fibre necrosis) developed more frequently in animals on diets deficient in thiamine than in animals on diets with normal or surplus thiamine, and more frequently in animals drinking alcohol and water than in those drinking water alone. No differences were observed between the different groups in the number of perivascular sympathetic nerves, in the motor nerve conduction velocities and in the muscle fibrillation potentials. Thus, thiamine deficiency, established as a significant reduction of red blood cell transketolase activity, seems to have a deleterious effect on the peripheral nerves and muscles. The effect is enhanced by the simultaneous consumption of ethyl alcohol.
Alcoholism↗
Diagnosis and management of brain death.
Finland was the first country in which brain death was legally accepted. Since 1975, 37 cases of brain death had been recorded in a university hospital in Finland, and these were reviewed. The cause for brain death was intracranial bleeding in 32 cases, other cerebrovascular disorder in two, and intracranial neoplasm in three. In 21 brain death was diagnosed clinically. In 16 cases confirmatory investigations (electroencephalography, cerebral angiography) were needed. After brain death had been established artificial support was withdrawn in 15 patients and organ transplantation was carried out in 10. In 12 patients, however, diagnosis of brain death did not influence management, though the heart stopped beating on average 25 hours after diagnosis. The Finnish criteria for brain death seem to be reliable and suitable for routine use.
Adolescent↗
Does ethanol intoxication promote brain infarction in young adults?
76 consecutive patients aged under 40 with ischaemic brain infarction verified by carotid angiography and/or serial brain scanning were studied. In at least 15 cases (20%) the onset of symptoms was preceded within 24 hours by a bout of alcohol drinking. Ethanol-related cases comprised 40%, 25%, and 13% of the patients in the age-groups 16-19, 20-29, and 30-39 years, respectively. Ethanol intoxication preceding the stroke was 2-3 times as common in male and 3-4 times as common in female patients as ethanol intoxication in the general Finnish population of the same ages and sex. Occasional ethanol intoxication seems to carry an increased risk of ischaemic brain infarction in young adults.
Adolescent↗
Clofibrate-induced myopathy in the rat.
Rats were given daily injections of 0.2 or 0.5 g/kg chlorophenoxyisobutyrate (clofibrate) for 9 to 46 days. Lower leg muscles were studied with light and electron microscopy. Daily treatment with 0.5 g/kg of the drug for 26--46 days caused myopathic changes.
Animals↗
Effects of ethanol on platelet function.
To obtain evidence for an ethanol mediated disruption of hemostasis we compared the effects of acute and chronic ethanol ingestion on platelet reactivity. Since ADP may be important for hemostasis in vivo it was used to induce platelet aggregation in platelet-rich plasma. Thromboxane B2 (TXB2) formed during the aggregation was measured by radioimmunoassay. Ethanol (1.5 g/kg) given to 8 healthy non-alcoholic male volunteers increased platelet reactivity to ADP and the associated TXB2 formation rose from 289 +/- 60 (mean +/- SE) to 984 +/- 263 fmol/10(7) platelets (p less than 0.025). The effects lasted for as long as ethanol was present in blood. In 13 non-cirrhotic male alcoholics the withdrawal of ethanol caused a 4-fold increase in TXB2 formation within one week but the basal levels before ethanol withdrawal were the same as in controls. These findings are discussed in relation to the higher risk of brain infarction seen in alcoholics and even associated with binge drinking. Further studies are needed to establish the effects of ethanol on prostacyclin formation.
Adenosine Diphosphate↗
Prevention of alcohol withdrawal seizures with carbamazepine and valproic acid.
To evaluate the value of the nonsedative anticonvulsants carbamazepine and valproic acid a controlled study including drug monitoring was carried out. Intoxicated alcoholics (n = 138) were admitted for inpatient detoxication and randomly assigned to either carbamazepine (n = 43), sodium valproate (n = 46) or placebo (n = 49) in a double-blind fashion. Drug treatment lasted for four days and the daily doses of both drugs amounted to 1200 mg in the beginning of the study. Sodium valproate induced gastric distress, nausea and vomiting more frequently than placebo. About half of the subjects had to stop carbamazepine because of intolerable side-effects including vertigo, nausea, vomiting, diplopia and rash. Serum carbamazepine levels (18-89 mumol/l) were found to be high (greater than 40 mumol/l) in many but not all of these subjects. Seizures occurred in 3 subjects on placebo, 2 on carbamazepine and 1 on sodium valproate. Delirium tremens developed in 2 on sodium valproate and 1 on placebo. The study demonstrates that drug side-effects may seriously hamper the utility of carbamazepine and sodium valproate as routine treatment for the prevention of alcohol withdrawal symptoms.
Adult↗
Effects of alcohol and the evening meal on shear-induced platelet aggregation and urinary excretion of prostanoids.
Moderate regular alcohol intake has been found to be associated with a decreased risk for coronary heart disease and stroke. We investigated the effects of acute intake of red wine (60 g ethanol) and a standard dinner under controlled conditions on haemostatic factors. Shear-induced platelet aggregation (SIPA) decreased after the intake of alcohol irrespective of whether the subjects were fasting or not, and also after the intake of food. The intake of alcohol inhibited the postprandial increase of von Willebrand factor multimers. Plasma levels of plasminogen activator inhibitor 1 activity (PAI-1) and serum triglycerides were increased by alcohol. Excretion of the platelet thromboxane A(2) metabolites 11-dehydrothromboxane B(2) and 2,3-dinorthromboxane B(2), as well as the endothelial prostacyclin metabolite 2, 3-dinor-6-ketoprostaglandin F(1)alpha, into urine was not influenced by either alcohol or food. We conclude that eating a dinner together with red wine has no untoward effect on SIPA and that the decrease of SIPA is not specific for alcohol.
Adult↗
Ethanol intoxication: a risk factor for ischemic brain infarction in adolescents and young adults.
Between January 1978 and December 1979 23 consecutive patients aged under 40 years with acute ischemic brain infarction were admitted to the department of neurology, Meilahti University Hospital in Helsinki. In 10 patients (43%) the onset of symptoms was preceded within 24 hours by ethanol intoxication, and all but one symptom occurred at weekends when most liquor is consumed in Finland. Ethanol intoxication preceding the stroke was 4 times as common in female and 5 times as common in male patients as ethanol intoxication in the general Finnish population of the same age and sex. The present results support those of our previous study and suggest that occasional ethanol intoxication increases the risk of ischemic brain infarction both in adolescents and young adults.
Adolescent↗
Ethanol intoxication: a risk factor for ischemic brain infarction.
One hundred consecutive patients (67 men, 33 women) aged from 15-55 with acute ischemic brain infarction verified by computed tomography and/or angiography and/or brain scanning were studied. In 40 cases the onset of symptoms was preceded within 24 hours by ethanol intoxication. Ethanol intoxication preceding brain infarction was 4-7 times as common in men and 6-15 times as common in women as ethanol intoxication in the general Finnish population of the same age and sex. Nineteen of the patients were heavy drinkers. Heavy drinking was twice as common in men and 5 times as common in women as heavy drinking in the general Finnish population of the same age and sex. Both occasional ethanol intoxication and regular heavy drinking seem to carry an increased risk of ischemic brain infarction. The ethanol-induced risk was highest in middle-aged women and young men.
Adolescent↗
Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke?
The effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B2 rose from 303 +/- 56 to 950 +/- 212 fmol per 10(7) platelets (p less than 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.
Adenosine Diphosphate↗