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Biomedical subjects

H Numminen

Publications and source records attributed to H Numminen.

At least 19 recordsLinked to original sources

Working memory and everyday cognition in adults with Down's syndrome.

A number of previous studies have suggested that young people with Down's syndrome (DS) have a specific deficit of the phonological loop component of the working memory. However, there have also been studies which have proposed a specific deficit of the central executive component of working memory and suggested similarities of working memory functioning with patients with Alzheimer's disease. Fifteen middle-aged people with DS were matched for their individual scores of non-verbal intelligence to 15 individuals with mixed aetiology of intellectual disability. A versatile range of tasks was used in order to evaluate the functioning of working memory components. In addition, several everyday cognition skills were assessed. The subjects with DS performed significantly more poorly in all tasks assessing the phonological loop. Performance in other working memory tasks and compound variables representing different working memory components was equal in the groups. In addition, both groups had equal everyday cognition skills. The functioning of the phonological loop seems to be clearly deficient in people with DS. Interestingly, the deficit does not seem to affect the vocabulary or other everyday cognition skills in individuals with DS. No signs of specific deficit of the central executive component of working memory were found.

Activities of Daily Living↗

Working memory structure and intellectual disability.

The working memory of people with intellectual disability has been found to generally lag behind their mental age. However, studies concerning the structure of working memory or its connections to other cognitive functions are rare. The present study employs a versatile battery of tests for the evaluation of working memory structure in adults with intellectual disability of unknown aetiology. In addition, connections between working memory and cognitive skills valid for everyday functioning are evaluated. Working memory performance in the study participants was found to stem from two distinct components which could be regarded to represent phonological and general working memory. General working memory was closely related to intelligence, whereas phonological working memory was not. The subjects in the study group differed in their working memory profiles. These distinct profiles were significantly related to academic skills (e.g. reading, writing and mathematics) and sentence comprehension because the profile of the working memory predicted these abilities even when the intelligence and educational background of the participants was taken into consideration.

Achievement↗

Decreased severity of brain infarct can in part explain the decreasing case fatality rate of stroke.

BACKGROUND AND PURPOSE: Case fatality rates for stroke has declined in most Western industrialized countries during recent decades. One possible explanation for this is a decrease in the severity of stroke symptoms. We therefore sought evidence for a change in stroke severity and its relationship with case fatality rates. METHODS: We compared the severity of symptoms among first-ever stroke patients in 2 population-based prospective stroke registers maintained during 1972 to 1973 and 1989 to 1991 in Finland. Patients who were evaluated by study assistants or the investigator during the first week after the onset of symptoms were included in the study, and their severity of symptoms was assessed with the use of comparable scales modified from the Scandinavian Stroke Scale. RESULTS: A total of 244 and 594 patients were registered, and a portion of them (155 [63.5%] and 360 [60.6%]) were included in the analyses in the registers for Espoo-Kauniainen from 1972 to 1973 and for 4 separate districts in Finland from 1989 to 1991, respectively. The death rates during the first week among those who were not included did not differ between the registers. The severity of symptoms decreased significantly between the registers in both patients with brain infarct or intracerebral hemorrhage but not in those with subarachnoid hemorrhage. The severity of symptoms was an independent factor of case fatality at 1 month. CONCLUSIONS: The severity of symptoms of brain infarcts has decreased and can in part explain the decreased case fatality rate of stroke in Finland. However, the change in patients with intracerebral hemorrhage may be overestimated due to undiagnosed intracerebral hemorrhages in the first register resulting from the lack of brain CT.

Aged↗

The effect of acute ingestion of a large dose of alcohol on the hemostatic system and its circadian variation.

BACKGROUND AND PURPOSE: Heavy binge drinking may trigger the onset of embolic stroke and acute myocardial infarction, but the underlying mechanisms are unclear. The effects of binge drinking on the hemostatic system and its circadian variation have not been investigated. We investigated the effects of an acute intake of a large dose of alcohol (1.5 g/kg). METHODS: Twelve healthy, nonsmoking men participated in sessions where they were served ethanol in fruit juice or served fruit juice alone and, lying in a supine position, were followed up for 12 to 24 hours. The treatments were randomized and separated from each other by a 1-week washout period. Blood and urine were collected for hemostatic measurements. RESULTS: The urinary excretion of the platelet thromboxane A(2) metabolite 2, 3-dinor-thromboxane B(2) was significantly (P<0.05) greater during the night after an evening intake of alcohol than during the control night. A smaller increase was observed during the daytime after an intake of alcohol in the morning. The effects on the endothelial prostacyclin metabolite 2,3-dinor-6-ketoprostaglandin F(1alpha) excretion were negligible. A 7-fold increase in plasminogen activator inhibitor 1 activity was observed after both morning (P<0. 05) and evening (P<0.01) intakes of alcohol. CONCLUSIONS: This is the first study to suggest that acute ingestion of a relatively large but tolerable dose of alcohol transiently enhances thromboxane-mediated platelet activation. The observations also demonstrate alcohol-induced changes in the normal circadian periodicity of the hemostatic system in subjects not accustomed to consumption of alcohol.

6-Ketoprostaglandin F1 alpha↗

Post-stroke depression and functional recovery in a population-based stroke register. The Finnstroke study.

Post-stroke depression and functional outcome were examined in a population-based stroke register active in four different districts (total population, 134 804) in Finland. Five hundred and ninety four first time strokes were registered. Beck's depression inventory (BDI), with ten as the cutoff point for depression, was applied to 321 of 423 survivors after three months and to 311 of 390 survivors after 12 months. Functional outcome was measured with the Barthel Index (BI) and the Rankin Scale (RS). One hundred and fifty one of 321 (47.0%) and 147 of 311 (47.3%) patients were depressed after three and 12 months, respectively. Depression at three months was associated with poor functional outcome at the one-year follow-up (P = 0.001 for the BI and the RS). On the other hand, poor functional outcome at three months was associated with depression after one year (P = 0.004 and 0.002 for the BI and the RS, respectively). Patients who were depressed at three months were more often in institutional care between three and 12 months later than non-depressed patients (P = 0.005). Post-stroke depression is associated with poor functional recovery of patients. If depression were diagnosed and treated early, it might help patients to recover more completely and/or faster, which could save community healthcare resources by avoiding or shortening the time of institutional care or reducing the need for home care.

Aged↗

Recent heavy drinking of alcohol and embolic stroke.

BACKGROUND AND PURPOSE: Epidemiological evidence suggests that heavy alcohol consumption increases the risk for ischemic stroke, whereas light-to-moderate alcohol intake decreases the risk, but the role of different drinking patterns has remained unclear. We investigated recent light, moderate, and heavy alcohol drinking and former heavy drinking as risk factors for acute ischemic brain infarction by etiological subtype of stroke. METHODS: We compared 212 consecutive patients aged between 16 and 60 years, who were completely evaluated for the etiology of their ischemic stroke, with 274 control subjects admitted to the emergency unit of the same hospital. ORs, as estimates of multivariate relative risks (RRs), and 95% CIs after adjustment for possible confounding variables were calculated by logistic regression. The ORs were adjusted for age, sex, body mass index, hypertension, diabetes, hyperlipemia, current smoking, and history of migraine. RESULTS: Recent heavy drinking but not former heavy drinking was an independent risk factor for stroke (RR 1.82, 95% CI 1.08 to 3.05). Consumption of 151 to 300 g and >300 g alcohol within the week preceding the onset of stroke significantly increased the risk for cardioembolic and cryptogenic stroke. Consumption of >40 g alcohol within the preceding 24 hours increased the risk for cardiogenic embolism to the brain among those who had a high-risk source (RR 4.75, 95% CI 1.23 to 18.4), the risk for tandem embolism among those who had prominent large-artery atherosclerosis (RR 7.68, 95% CI 1.82 to 32.3), and the risk for cryptogenic stroke (RR 3.84, 95% CI 1.69 to 8.71). Light drinking did not increase the risk for stroke. CONCLUSIONS: We conclude that acute drinking of intoxicating amounts of alcohol may trigger the onset of embolic stroke among subjects who have a source of thrombus in the heart or the large arteries.

Adolescent↗

Alcohol intake and the risk of stroke.

Alcohol consumption has been reported to have both beneficial and harmful effects on the incidence of stroke. Different drinking habits may explain the diversity of the observations, but this is still unclear. We reviewed recent clinical and epidemiological studies to find out whether alcohol intake could increase or decrease the risk for stroke. By a systematic survey of literature published from 1989 to 1997, we identified 14 case-control studies addressing alcohol as a risk factor for haemorrhagic and ischaemic stroke morbidity and fulfilling the following criteria: the type of stroke was determined by a head computerised tomography scan on admission or at autopsy; and alcohol consumption was verified using structured questionnaires or by personal interviews. In some studies, adjustment for hypertension abolished the independent role of alcohol as a risk factor. On the other hand, the studies covering even recent alcohol intake showed in many cases that heavy drinking is an independent risk factor for most stroke subtypes, and that the risk may decrease relatively rapidly after the cessation of alcohol abuse. In some studies, regular light to moderate drinking seemed to be associated with a decreased risk for ischaemic stroke of atherothrombotic origin. In conclusion, recent heavy alcohol intake seems to be an independent risk factor for all major subtypes of stroke. The ultimate mechanisms leading to the increased risk are unclear. The significance of alcohol as a risk factor has been demonstrated in young subjects because they are more often heavy drinkers than the elderly. Several factors to explain the beneficial effect of light to moderate drinking have been proposed.

Alcohol Drinking↗

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↗

Depression after stroke: results of the FINNSTROKE Study.

BACKGROUND AND PURPOSE: We compared the incidence and severity of depression at 3 and 12 months after stroke in patients and their chief caregivers (spouses, 63%; children, 37%) in four districts of Finland, two with and two without after-hospital-discharge interventional programs (outpatient rehabilitation and activities of the local divisions of the Finnish Heart Association [FHA]). A population-based stroke register was used, and factors influencing depression were analyzed. METHODS: A stroke register of patients recruited over 2 years in four different districts (total population, 134804) in Finland; 594 first-ever strokes were registered. Beck's Depression Inventory (BDI), with 10 as the cutoff point for depression, was applied to 321 of 423 survivors and 195 caregivers at 3 months and to 311 of 390 survivors and 184 caregivers at 12 months in the districts with and without interventional programs. RESULTS: At 3 months, fewer patients in the districts with active programs (41%) were depressed than in the control districts (54%) (odds ratio, 0.59; 95% confidence interval, 0.37 to 0.94), and the difference was maintained at 12 months (42% versus 55%) (odds ratio, 0.55; 95% confidence interval, 0.34 to 0.88). Univariate risk factors for depression at 3 months were female sex and severe prognostic score at the onset of stroke (< or = 14 points) on the Scandinavian Stroke Scale (SSS). Only SSS prognostic score and age emerged as significant independent contributors to depression on both linear and logistic multivariate analyses. There was no significant difference in the depression rate of caregivers between districts with active programs (42%) and those without such programs (41%) at 3 months; at 12 months the results were the same (39% in districts with active programs versus 42% in those without such programs). However, at 12 months there were significantly more severely depressed caregivers in districts without active programs than in districts with such programs (P.036). Poor Rankin scale score (grades III through V) and severe SSS long-term score (< or = 42 points) at 3 months among the patients were associated with depression of the caregivers at 3 months in the univariate analysis. Poor Rankin Scale score of the patients was independently associated with the depression of their caregivers at 3 months on multivariate logistic regression analysis. CONCLUSIONS: Depression was common among stroke survivors and among their caregivers at 3 months, and its rate did not decrease at 1-year follow-up. The lower depression rate in districts with active programs compared to those without supports the idea that outpatient rehabilitation and support provided by local divisions of the FHA may be an effective way of decreasing the rate of depression after stroke.

Aged↗

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↗

Declining incidence and mortality rates of stroke in Finland from 1972 to 1991. Results of three population-based stroke registers.

BACKGROUND AND PURPOSE: We aimed to determine trends in stroke incidence, mortality rates, case-fatality rates, and their relation in Finland. METHODS: We compared the results of three population-based stroke registers that included first-ever strokes in people aged > or = 15 years. Two registers were kept in Espoo-Kauniainen, the first in 1972 to 1973 (EK 72-73) and the second in 1978 to 1980 (EK 78-80). The present register of the Finnish Heart Association (FHA 89-91) was kept in four districts in Finland in 1989 to 1991. RESULTS: The age-adjusted incidence rates were 240.9, 174.4, and 191.6, and the 1-year mortality rates were 121.9, 77.0, and 65.3 in the EK 72-73, EK 78-80, and FHA 89-91 registers, respectively. The overall decline from 1972 to 1991 was 20% in the stroke incidence rate and 46% in the stroke mortality rate. One-month case-fatality rates decreased from 34.8% to 29.4% in the EK 72-73 and EK 78-80 registers and to 23.3% in the present register. CONCLUSIONS: The decline in the stroke incidence rate during the 1970s stabilized during the late 1980s and early 1990s; however, the case-fatality rate is still decreasing. Their combined effects may explain the continuing decline in stroke mortality.

Adolescent↗

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↗

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↗

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↗

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↗

Combined effect of a small dose of ethanol and 36 hr fasting on blood-glucose response, breath-acetone profiles and platelet function in healthy men.

Six healthy men drank 0.25 g/kg ethanol after an overnight fast (12 hr) and the same dose was consumed again after a further 24 hr fasting. The concentration of ethanol and acetone in end-expired alveolar air was determined at 15 min intervals for 3 hr after ethanol intake by a gas chromatographic method. Before drinking and 30 and 90 min thereafter blood samples were taken for determination of glucose, ADP-induced platelet aggregation and associated thromboxane (TXB2) formation. The breath-ethanol time course was virtually identical after 12 and 36 hr fasting and the peak concentration occurred 30 min after drinking. Fasting for 36 hr caused a 20-fold increase in breath-acetone levels. Under these conditions, i.e. after 12 and 36 hr fasting, the hypoglycemic response to ethanol intake was 10 and 25%, while the antiketogenic response was 38 and 16%, respectively. ADP-induced platelet aggregation and associated TXB2 formation showed wide interindividual variations, but no definite effects of ethanol, hypoglycemia or metabolic acidosis were observed. Platelet function was not significantly influenced by ingestion of a small dose of ethanol after prolonged fasting.

Acetone↗

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↗

Tower of Hanoi and working memory in adult persons with intellectual disability.

Persons with intellectual disability (ID) have been found to perform more poorly than their mental age would suggest in the visuo-spatial problem solving task Tower of Hanoi (TOH). Inefficient performance has been assumed to be related to inability to use sophisticated problem solving strategies because of restricted working memory capacity. In the present study, the TOH performance of adult persons with ID was found to be equal to that of fluid-intelligence-matched general children. However, persons with ID violated the rules of the TOH more often, and needed more trials to solve the TOH problems than the children did. Visuo-spatial and executive working memory tasks were significantly connected to the TOH performance of persons with ID, whereas phonological working memory tasks were not. Poor inhibition ability was related to the poor performance of subjects with ID in the TOH. We suggest that for persons with ID, TOH performance is determined by individual differences in fluid intelligence, controlled attention, and inhibition ability.

Adult↗