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M Hillbom

Publications and source records attributed to M Hillbom.

At least 37 records · Page 2Linked to original sources
PubMed1998

Mechanisms of alcohol-related strokes.

Epidemiological investigations have shown a linear positive correlation between the risk of haemorrhagic stroke and level of alcohol consumption. Ischaemic stroke shows a weaker relationship, which is J-shaped, suggesting that regular light-to-moderate alcohol consumption may carry a decreased risk. Case reports and case-control studies indicate that heavy recent drinking, but not heavy former drinking, increases the risk for both types of stroke. Larger amounts of alcohol are needed to trigger aneurysmal subarachnoid haemorrhage than spontaneous intracerebral haemorrhage. The increased risk caused by recent heavy drinking may be partly due to elevated systolic blood pressure, but alcohol may also provoke cerebral arterial vasospasm, as observed in animal experiments. Alcohol-induced fluctuation in haemostatic and fibrinolytic factors has not been proved to precipitate alcohol-related strokes, but may contribute to both an increase and a decrease of the risk. Subtypes of ischaemic stroke associate differently with alcohol consumption. A recent series of patients with ischaemic brain infarction showed that of the victims having a high and medium risk for cardiogenic embolism, 50% and 45% were intoxicated, respectively. This suggests that cardiogenic embolism is a significant mechanism leading to ischaemic stroke during heavy drinking of alcohol.

Adult↗
PubMed1998

Alcohol consumption and stroke: benefits and risks.

The complex relationship between alcohol consumption and stroke includes both benefits and risks. Regular light-to-moderate consumption of alcohol seems to decrease the risk for ischemic stroke by reducing atherothrombotic events, but the underlying mechanism is still unclear. Recent and current (but not previous) heavy drinking increases the risk for both hemorrhagic and ischemic strokes. Young and middle-aged men are stricken more often than women or elderly persons, probably because they are more often current heavy drinkers. Alcoholic cardiomyopathy is a cause of cardioembolic brain infarction. Cardiac arrhythmias caused by regular heavy drinking or binge drinking can precipitate thrombus formation and propagate already existing thrombi from the heart. The maintenance of high blood pressure by heavy drinking may promote cerebral arterial degeneration, but the effect of drinking habits on aneurysm formation is not known. Acute increases in systolic blood pressure and/or alterations in cerebral arterial tone could serve as mechanisms triggering hemorrhagic strokes during alcoholic intoxication. We lack studies to show that prevention of heavy drinking can efficiently influence the occurrence of strokes.

Adult↗
PubMed1998

Dye dilution and oximetry for detection of patent foramen ovale.

OBJECTIVES: Patent foramen ovale (PFO) is a risk factor for stroke of undetermined (cryptogenic) origin. Low cost and non-invasive bedside tests for detection of PFO are needed as alternatives to contrast transesophageal echocardiography. We investigated whether dye dilution curves and oximeter recordings are useful for detecting PFO and what is the prevalence of PFO in patients with cryptogenic stroke determined with these bedside methods. We also studied whether stroke risk factors, number of brain lesions, and stroke recurrence rates were different in patients with an unexplained stroke with and without PFO. MATERIAL AND METHODS: Dye dilution curves and oximeter recordings with non-invasive earpiece apparatus were obtained in 59 patients aged under 50 years who had had a cryptogenic brain infarction. The number of ischemic lesions in the brain was counted by MRI. RESULTS: PFO was found in 24 (41%) of 59 patients. There was a 100% concordance in results obtained by dye dilution and by oximetry. Risk factors for stroke were similar in subjects with PFO and those without PFO. No significant association was found between PFO and Valsalva-like activity at stroke onset. Those with PFO did not have more ischemic lesions detected by MRI nor did they have more recurrent ischemic episodes. CONCLUSION: Dye dilution and oximetry are cheap and useful methods for detection of PFO and could be used for screening of the risk of paradoxical embolism. Because these 2 methods were not compared with the golden standard, transesophageal echocardiography, the specificity and sensitivity of the tests remain unsettled.

Adolescent↗
PubMed1998

Alcohol and stroke: pathophysiologic mechanisms.

Epidemiological evidence indicates that recent heavy alcohol consumption increases the risk for all major types of stroke, whereas light-to-moderate alcohol intake is associated with a decreased risk of ischemic stroke. Although heavy drinking elevates blood pressure, there is no firm evidence to indicate that alcohol consumption causes the formation of aneurysms, microaneurysms or other lesions in human arteries. Alcohol has been reported to precipitate vasoconstriction and rupture of small cerebral arteries in experimental animals. Alcohol-induced neck trauma has been shown to precipitate traumatic strokes, and alcohol-induced cardiac arrhythmias have been observed in patients with embolic brain infarction. The effects of alcohol on hemostasis, fibrinolysis and blood clotting are variable and could either prevent or promote the occurrence of strokes. The antiatherogenic effects of regular light-to-moderate alcohol consumption could be mediated by inhibition of low-density lipoprotein oxidation, and by elevated estrogen levels.

Alcohol Drinking↗
PubMed1997

Lifestyle-associated risk factors for acute brain infarction among persons of working age.

BACKGROUND AND PURPOSE: This study was designed to identify whether cigarette smoking, alcohol drinking, obesity, and use of oral contraceptives are independent risk factors for brain infarction among persons of working age. METHODS: Health habits and previous diseases of 506 patients (366 men and 140 women aged 16 to 60 years) with acute first-ever symptomatic brain infarction were compared with those of 345 hospitalized control patients (219 men and 126 women) who did not differ from case subjects in respect to day of onset of symptoms or acuteness of disease onset. With the use of stepwise logistic regression, the variables for which the simultaneous risks of acute brain infarction were tested by sex were age, amount of alcohol consumed within 24 hours and 1 week before the illness, heavy drinking, smoking status, current smoking, cardiac disease, hypertension, diabetes, hyperlipemia, migraine, body mass index, and, in women, current use of oral contraceptives. RESULTS: Intake of > 40 g ethanol within the 24 hours preceding the onset of illness increased the risk for acute brain infarction both among men (P < .001) and women (P < .01) independently from other risk factors. Other significant independent risk factors for brain infarction among men were hypertension (P < .001), cardiac disease (P < .01), current smoking (P < .01), diabetes (P < .05), and history of migraine (P < .05) and among women, current use of oral contraceptives (P < .01) and current smoking (P < .05). CONCLUSIONS: Recent heavy drinking of alcohol, hypertension, cardiac disease, current smoking, diabetes, and history of migraine among men, and recent heavy drinking of alcohol, current use of oral contraceptives, and current smoking among women, seem to be independent risk factors for acute brain infarction.

Adolescent↗
PubMed1996

Platelets, alcohol consumption, and onset of brain infarction.

OBJECTIVES: Previous investigations have suggested that recurrent rebound thrombocytosis after alcohol misuse may be a factor in the pathogenesis of thromboembolic disease. Alcohol consumption, platelet count, and platelet function were examined among patients of working age with brain infarction. METHODS: Platelet count and risk factors for stroke were studied in 426 stroke patients and 157 control patients in hospital. The measures were platelet count obtained within four days after the stroke onset, in vitro adenosine diphosphate induced platelet aggregation, associated thromboxane B2 formation, and urinary excretion of 11-dehydrothromboxane B2. RESULTS: After adjustment for sex, age, cardiac disease, diabetes, and alcohol intake, hypertension (OR 3.4, 95% confidence interval (95% CI) 2.0-6.0) and current smoking (OR 2.1, 95% CI 1.4-3.3) were associated with an increased risk for brain infarction. Platelet count shortly after the onset of disease was higher in the stroke patients than in the controls (OR 1.05/10(10)/1 platelets; 95% CI 1.02-1.09). The patients with brain infarction who were heavy alcohol drinkers (n = 144) showed both thrombocytosis (OR 2.30, 95% CI 0.82-6.44) and thrombocytopenia (OR 3.20, 95% CI 1.19 to 8.59) more often at the onset of the stroke than the other patients with brain infarction. The thromboxane variables showed inconsistent associations with the onset of stroke. There was no consistent platelet abnormality among alcohol misusers at the onset of ischaemic brain infarction. CONCLUSIONS: Alcohol induced thrombocytopenia and rebound thrombocytosis were both often seen at the onset of brain infarction in patients who were heavy alcohol drinkers. Therefore, other mechanisms which could contribute to the high frequency of recurrences of ischaemic stroke among heavy drinkers should be investigated.

Adenosine Diphosphate↗
PubMed1996

Weekend and holiday increase in the onset of ischemic stroke in young women.

BACKGROUND AND PURPOSE: Chronobiological analyses of stroke onset may throw some light on the mechanisms that trigger stroke. Observations may generate new hypotheses for identifying significant causal relationships. METHODS: In the present study, both the circadian and the weekend and holiday versus workday times of the onset of ischemic cerebral infarction were determined for 723 consecutive subjects, aged 16 to 60 years, who were admitted for hospital treatment in the acute phase without any selection. RESULTS: Among young adults (16 to 40 years) and women, more infarctions occurred during weekends and holidays than were expected. Young women in particular had an increased risk for brain infarction during weekends and holidays (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.26 to 3.63). In a multivariate analysis, age of 16 to 30 years (OR, 3.13; 95% CI, 1.57 to 6.50), female sex (OR 1.71; 95% CI, 1.12 to 2.63), and recent drinking of alcohol (P < .01) were associated with the onset of brain infarction during weekends and holidays, whereas current cigarette smoking was associated with the onset of brain infarction during workdays (P < .001). A morning increase in the onset of brain infarction was observed among middle-aged people during both weekends/holidays and workdays. Among young adults, however, an evening increase was also seen during weekends/holidays and workdays. CONCLUSIONS: We found that young adults and women are frequently stricken by brain infarction during weekends and holidays and that the circadian distribution of the onset of brain infarction among young adults is different from that of middle-aged people. These observations suggest that there may be stroke-triggering activities that are associated with lifestyle.

Adolescent↗
PubMed1995

Recent alcohol consumption, cigarette smoking, and cerebral infarction in young adults.

BACKGROUND AND PURPOSE: The role of recent heavy drinking of alcohol as a risk factor for ischemic brain infarction is unclear. We investigated this problem in young adults, in whom even a thorough workup often fails to reveal any predisposing factor. METHODS: This was a hospital-based case-control study comprising 75 consecutive subjects aged 16 to 40 years with first-ever ischemic brain infarction and 133 control subjects from the same hospital who were group-matched with the case patients for age, sex, day of the onset of symptoms, and acuteness of disease onset. RESULTS: Multiple logistic regression analysis showed that alcohol intake exceeding 40 g of ethanol within the 24 hours preceding disease onset was a significant independent risk factor for brain infarction among both men (odds ratio [OR], 6.0; 95% confidence interval [CI], 1.8 to 20.3) and women (OR, 7.8; 95% CI, 1.0 to 60.8). Cigarette smoking was not found to be an independent risk factor in the model, whereas among men arterial hypertension was (OR, 6.2; 95% CI, 1.5 to 24.7). CONCLUSIONS: We conclude that very recent alcohol drinking, particularly drinking for intoxication, may trigger the onset of brain infarction in young adults and that there might be a variety of mechanisms behind this effect.

Adolescent↗
PubMed1995

Risk factors for spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Spontaneous intracerebral hemorrhage has remained a serious disease despite recent improvements in medical treatment. This study was designed to identify modifiable risk factors for intracerebral hemorrhage. METHODS: Health habits, previous diseases, and medication of 156 consecutive patients with intracerebral hemorrhage aged 16 to 60 years (96 men and 60 women) were compared with those of 332 hospitalized control patients (192 men and 140 women) who did not differ from case subjects in respect to age, day of onset of symptoms, or acuteness of disease onset. RESULTS: After adjustment for sex, age, hypertension, body mass index, smoking status, and alcohol consumption during the last week, patients who had consumed 1 to 40, 41 to 120, or > 120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk (95% confidence interval) of hemorrhage of 0.3 (0.2 to 0.7), 4.6 (2.2 to 9.4), and 11.3 (3.0 to 42.8), respectively, compared with those who had consumed 0 g. In addition, alcohol intake within 1 week before the onset of illness, excluding use within the last 24 hours, increased the risk of hemorrhage; adjusted risks were 2.0 (1.1 to 3.5) for 1 to 150 g, 4.3 (1.6 to 11.7) for 151 to 300 g, and 6.5 (2.4 to 17.7) for > 300 g compared with 0 g. The adjusted risk of hypertension for hemorrhage was 6.6 (3.9 to 11.3). Previous heavy alcohol consumption and current cigarette smoking were not independent risk factors for hemorrhage, but anticoagulant treatment was (P < .01). Erythrocyte mean corpuscular volume and gamma-glutamyl transferase values were also higher in patients with intracerebral hemorrhage than in control subjects. CONCLUSIONS: Recent moderate and heavy alcohol intake as well as hypertension and likely also anticoagulant treatment seem to be independent risk factors for intracerebral hemorrhage.

Adolescent↗
PubMed1994

Neurological recovery after liver transplantation: a prospective study of 22 patients.

A group of 22 liver transplantation patients were examined pre- and postoperatively using clinical neurological, neurophysiological and neuroradiological methods. After the operation improvement was observed in neurological symptoms, and in neuropsychological and neurophysiological test results. Our study shows that liver recipients have a high prevalence of nervous system dysfunction and that successful transplantation is followed by significant improvement.

Adult↗
PubMed1994

Increased urinary excretion of a major thromboxane metabolite in early alcohol withdrawal.

Urinary excretion of 2,3-dinor-thromboxane B2 as a marker of in vivo thromboxane A2 (TxA2) biosynthesis was measured in six alcoholics 1 and 14 days after the cessation of heavy drinking using gas chromatography/mass spectrometry. Six non-alcoholic healthy volunteers served as controls. One day after alcohol withdrawal the excretion of the dinor metabolite was significantly higher (P < 0.01) in the alcoholics (408 +/- 42 pg mg-1 creatinine) than in the controls (180 +/- 30 pg mg-1 creatinine) and was accompanied by a significantly reduced platelet count (103.0 +/- 20.2 x 10(9) l-1 vs. 194.0 +/- 13.9 x 10(9) l-1 in controls; P < 0.01). The metabolite excretion fell then significantly (P < 0.05) to 245 +/- 53 pg mg-1 creatinine 14 days after alcohol withdrawal and this was paralleled by an increase in platelet count to 453.5 +/- 72.0 x 10(9) l-1 (P < 0.05). The present results support the hypothesis that Tx-A2 biosynthesis is increased in early alcohol withdrawal and strongly suggest platelets as a cellular origin of the increased TxA2 formation.

Adult↗
PubMed1993

Cigarette smoking and alcohol consumption as risk factors for aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Aneurysmal subarachnoid hemorrhage is a serious disease despite recent improvements in medical and surgical treatment. Hence, identification of modifiable risk factors for subarachnoid hemorrhage is important. METHODS: We compared the smoking and drinking habits of 278 consecutive patients with aneurysmal subarachnoid hemorrhage, aged 15-60 years (145 men and 133 women) with those of 314 hospitalized control patients (164 men and 150 women) who did not differ in regard to age, day of onset of symptoms, and acuteness of disease onset. RESULTS: Multiple logistic regression analysis showed that recent alcohol intake and smoking, but not hypertension, were significant independent risk factors for hemorrhage. After adjustment for age, hypertension, and smoking status, men who had consumed 1-40, 41-120, or > 120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk of hemorrhage of 0.3 (95% confidence interval [CI], 0.1-0.8), 2.5 (95% CI, 1.1-5.5), and 4.5 (95% CI, 1.5-12.9), respectively, compared with men who had consumed 0 g. Women who had consumed 1-40 or > 40 g of alcohol had a risk of hemorrhage of 0.4 (95% CI, 0.2-0.8) and 6.4 (95% CI, 2.3-17.9), respectively, compared with women without use of alcohol. Heavily smoking (> 20 cigarettes per day) men and currently smoking women had adjusted relative risks of hemorrhage of 7.3 (95% CI, 3.8-14.3) and 2.1 (95% CI, 1.2-3.6), respectively, compared with men who had never smoked and with women who were not current smokers. Higher levels of erythrocyte mean corpuscular volume in patients with subarachnoid hemorrhage than in control subjects supported the notion of different smoking and drinking habits. CONCLUSIONS: Recent heavy alcohol intake and current smoking seem to be independent risk factors for aneurysmal subarachnoid hemorrhage.

Adolescent↗
PubMed1992

Encephalopathy and neuropathy in end-stage liver disease before and after liver transplantation.

The nervous system involvement of 8 patients with end-stage liver disease was evaluated by means of clinical neurological, neuropsychological, neurophysiological and neuroradiological investigation before and 6-12 months after a successful liver transplantation. Preoperatively, all subjects (7 women, 1 man; mean age 40 years, range 30-54 years) exhibited decreased muscle strength and 2 patients manifested clinical signs of polyneuropathy. In neuropsychological tests, slight visuoconstructive apraxia, and disturbances of verbal memory and cognitive function were observed. Magnetic resonance imaging (MRI) revealed cerebral lesions in two patients. After transplantation, muscle strength reverted to normal in all patients, polyneuropathy improved and in all but 2 patients recovery of neuropsychological functioning was observed. Clinical signs of encephalopathy had disappeared. All patients were emotionally better adjusted after transplantation. Four subjects showed new, albeit mild changes in neurophysiological and neuropsychological tests postoperatively. We conclude that the majority of neurological impairment disappeared after liver transplantation. We want to stress that evaluation of neurological sequelae of liver transplantation needs to be based on assessments both before and after liver transplantation.

Adult↗
PubMed1991

Effects of exercise and ethanol ingestion on platelet thromboxane release in healthy men.

We studied the effects of repeated bicycle exercises and ethanol ingestion (1.5 g/kg) on platelet aggregation and thromboxane (TxB2) release in 10 healthy male volunteers. After a bicycle exercise performed in the morning, the adenosine diphosphate (ADP)-induced platelet aggregation and the aggregation-associated thromboxane release were found to be decreased in fasting men. In contrast, after ingestion of fruit juice and a second exercise at noon, platelet aggregation and thromboxane release were increased. These latter changes were negligible when ethanol was ingested together with fruit juice. A third exercise, performed in the evening, again caused a decrease in the aggregation and associated thromboxane release during the control session, but provoked an increase during the ethanol session. Exercise increased the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha. Changes in the plasma arachidonic acid (AA) concentration probably influenced the platelet thromboxane release. The results suggest that both physical exercise and ingestion of ethanol in fruit juice influence the ADP-stimulated platelet thromboxane release.

Adenosine Diphosphate↗
PubMed1991

Platelet thromboxane release and delayed cerebral ischemia in patients with subarachnoid hemorrhage.

Adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release were studied in 52 patients with subarachnoid hemorrhage (SAH) in order to detect a possible association between altered platelet function and development of cerebral ischemic complications after SAH. Compared to the values on admission, the patients showed significantly increased platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001) 1 to 2 weeks after SAH. The highest values of thromboxane release were seen in patients who deteriorated due to delayed cerebral ischemia with a permanent neurological deficit. Thromboxane release was significantly higher (p less than 0.05) before the onset of severe delayed ischemia in six patients with preoperative ischemia compared to the patients without delayed ischemia. In five others, both ischemic deterioration and elevated thromboxane release occurred after operation. These patients had preoperative values similar to the values in those without ischemic symptoms. The observations suggest that increased platelet aggregability and thromboxane release are associated with delayed cerebral ischemia both before and after surgery.

Adult↗
PubMed1990

Platelet thromboxane release after subarachnoid hemorrhage and surgery.

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in platelet-rich plasma from 88 patients with subarachnoid hemorrhage and 26 healthy controls. During the first 3 days after subarachnoid hemorrhage, the patients showed significantly decreased (p less than 0.05) platelet aggregability and thromboxane release relative to the controls, but these effects disappeared in a few days. Platelet count increased for 3 weeks after subarachnoid hemorrhage. Surgery in 67 patients was followed by significant increases in platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001). Greatest thromboxane release was found in the eight patients showing delayed (postoperative) ischemic deterioration with a permanent neurologic deficit. Although platelet hyperaggregability and increased thromboxane release were particularly prominent in these eight patients, the role of these hematologic parameters in the pathogenesis of delayed ischemic deterioration remains unclear.

Adult↗
PubMed1990

Effect of nimodipine on platelet function in patients with subarachnoid hemorrhage.

We studied platelet function in 41 patients with subarachnoid hemorrhage who were randomized to receive either nimodipine or placebo in a double-blind fashion. Nimodipine was given to 21 patients, intravenously for 7-10 days and then orally until 21 days after the subarachnoid hemorrhage. The other 20 patients received placebo in a similar manner. Nimodipine did not significantly influence platelet aggregability. For the first 1-5 days after the subarachnoid hemorrhage, nimodipine treatment did not have any notable effect on adenosine diphosphate-induced platelet thromboxane B2 release, but a significant (p less than 0.05) inhibitory effect was observed thereafter. During intravenous administration, nimodipine prevented the increase in thromboxane release otherwise observed after subarachnoid hemorrhage. Concomitant with the decrease in thromboxane release, nimodipine increased the platelet count both before and after surgery so that the capacity for thromboxane formation per liter of blood decreased less than expected on the basis of thromboxane release per 10(7) platelets. Our study suggests that nimodipine might diminish the chance of cerebral ischemia by inhibiting platelet thromboxane release.

Adult↗