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Biomedical subjects

G Boysen

Publications and source records attributed to G Boysen.

At least 37 records · Page 2Linked to original sources
PubMed2001

[Intervention for apoplexy patients discharged from hospital. Psychosocial support: a literature review].

Psychosocial support has been suggested as a way of easing stroke survivors' and their carers' adjustment to a life with disability. The literature on psychosocial support services following primary rehabilitation in hospital was reviewed. Eleven controlled studies evaluating the effect of psychosocial support interventions after discharge from hospital were identified. The studies differed widely with respect to design, intervention and evaluation methods. The results suggest that psychosocial support after discharge can improve psychological well being and quality of life for stroke survivors and their families and improve the social activity of patients. The effect was achieved by using different types of intervention such as providing information, counselling and support from stroke clubs. Psychosocial support for carers was effective as well. Future research should elucidate this area, including evaluation of psychosocial support as a tertiary prevention strategy.

Adaptation, Psychological↗
PubMed2001

[Intervention for apoplexy patients discharged from hospital. Physical training: a literature review].

Stroke is among the leading causes of disability in Denmark. Rehabilitation services are in the process of being reorganised into dedicated stroke units. There is a general tendency toward reduction of length of in-patient treatment. The literature on outpatient rehabilitation services following primary rehabilitation on an inpatient basis was reviewed. The results of 16 randomised studies indicate that: 1) Continued rehabilitation after discharge can improve functional capacity of disabled stroke survivors; 2) Home-based rehabilitation is as effective as hospital-based outpatient rehabilitation; 3) Early supported discharge (ESD) services can reduce length of hospital stay but the relative advantages and drawbacks remain unclear. Ongoing rehabilitation by teams specialised in stroke rehabilitation seems to be crucial. More research, including evaluation of home-based rehabilitation services, is called for and existing outpatient rehabilitation services should be evaluated scientifically.

Activities of Daily Living↗
PubMed2001

Lung function and risk of fatal and non-fatal stroke. The Copenhagen City Heart Study.

BACKGROUND: Reduced lung function has been shown to be a significant predictor of non-fatal ischaemic heart disease, and of mortality due to cardiovascular disease. Fewer studies have analysed the relationship between lung function and risk of fatal or non-fatal stroke. The present study presents results on the relation between forced expiratory volume in one second (FEV1) and risk of incident and fatal first-ever stroke. SUBJECTS AND METHODS: The analyses are based on prospective cohort data from 12 878 eligible men and women aged 45-84 years, who participated in the first health examination of the Copenhagen City Heart Study in 1976-1978. The subjects were followed from day of entry until 31 December 1993. During that period 808 first-ever strokes occurred of which 153 were fatal within 28 days. Risk of incident and fatal stroke was estimated by means of Cox hazard regression. The analyses included adjustment for potential confounders: sex, age, smoking, inhalation, body mass index, systolic blood pressure, triglycerides, physical activity in leisure time, education, diabetes mellitus, and antihypertensive treatment. RESULTS: We found an inverse association between FEV1 and risk of first-time stroke. For each 10% decrease in FEV1 in percentage of expected, the relative risk (RR) increased 1.05 (95% CI : 1.00-1.09, P = 0.03). This represents an approximately 30% higher risk of stroke in the group of people with the lowest lung function as compared to the group with the highest lung function. The association between lung function and risk of fatal stroke resembled that of risk of incident stroke (fatal and non-fatal). The RR was 1.11 (95% CI : 1.03-1.19) for each 10% decrease in FEV1 in percentage of expected. This represents approximately a doubling of the risk between the highest and lowest lung function groups. CONCLUSIONS: This study shows that reduced lung function measured in percentage of predicted FEV1 is a predictor of first-time stroke and fatal stroke independent of smoking and inhalation. The high risk of fatal first-ever stroke in the group of people with low lung function may be of significance in both the design and interpretation of clinical trials.

Aged↗
PubMed2001

Stroke severity determines body temperature in acute stroke.

BACKGROUND AND PURPOSE: Several studies have claimed that temperature on admission is of prognostic significance in acute stroke. Experimental studies showing that hyperthermia increases infarct size have lent credibility to this assumption. The aim of the present study was to test the hypothesis that initial body temperature is of importance for stroke outcome. METHODS: This prospective study included 725 consecutive patients, 584 with cerebral infarcts and 141 with intracerebral hemorrhages, admitted to an acute stroke unit within 6 hours of stroke onset. Time of stroke onset and time of admission were recorded. Body temperature was measured on admission and every 2 hours during the first 24 hours. Patients were divided into 2 groups on the basis of stroke severity on admission: Scandinavian Stroke Scale Score (SSS) </=25 was defined as major stroke, and SSS >25 was defined as mild to moderate stroke. RESULTS: On admission, mean body temperature was normal. In the major stroke patients, body temperature started to rise 4 to 6 hours after stroke onset. At 10 to 12 hours after stroke onset, increased body temperature was found to be related to poor outcome. In mild to moderate stroke, there was no significant rise in temperature. Initial temperature >37.5 degrees C was not related to stroke severity or stroke outcome. CONCLUSIONS: In major stroke, a significant rise in temperature occurred hours after stroke onset. Severe infarcts and intracerebral hemorrhages caused temperature to rise, whereas initially increased temperature had no influence on stroke severity. Elevated body temperature on admission within 6 hours of stroke onset had no prognostic influence on stroke outcome at 3 months.

Acetaminophen↗
PubMed2000

[An awful story].

Explore the source record for details and available documents.

Cost Savings↗
PubMed2000

Glycerol for acute ischaemic stroke.

BACKGROUND: Infarct-related oedema following ischaemic stroke is thought to be a major cause of early death. Intravenous glycerol may reduce the oedema, increase cerebral blood flow and improve cerebral metabolism. OBJECTIVES: The objective of this review was to assess the effect of glycerol in acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register, Medline and Embase. SELECTION CRITERIA: Randomised trials of intravenous glycerol compared with control in people with definite or presumed ischaemic stroke. Trials were included if treatment was initiated within the first four days of stroke onset. DATA COLLECTION AND ANALYSIS: Two reviewers assessed trial quality and independently extracted the data. MAIN RESULTS: Eight trials involving 649 people were included. Based on 454 patients in six trials, glycerol was associated with a decrease in deaths within 14 days of stroke onset (odds ratio of 0.58, 95% confidence interval 0.36 to 0.91). Based on 431 patients in five trials, there was a non-significant decrease in deaths within the first year of stroke onset (odds ratio of 0.82, 95% confidence interval 0.54 to 1.23). The effect of treatment on functional outcome was not clear. Haemolysis appeared to be the only adverse effect. REVIEWER'S CONCLUSIONS: There is not enough evidence to evaluate glycerol treatment for people with acute ischaemic stroke.

Brain Edema↗
PubMed2000

Prevention of recurrent stroke.

There is a considerable knowledge about risk factors for first ever stroke and a lack of knowledge about risk factors for recurrent stroke. As neurologists we rarely see the patient before the first transient ischemic attack (TIA) or stroke, and we are concerned with and need data on secondary stroke prevention. For lifestyle factors such as cigarette smoking, physical activity and alcohol consumption, data are scarce. For post-menopausal estrogen use there are no data on risk of recurrent stroke. Plasma homocysteine has emerged as a risk factor for stroke and cardiovascular disease. It is not yet documented if supplementation of folic acid, which may reduce plasma homocysteine, also lowers risk of stroke. Elevated blood pressure is a risk factor for recurrent stroke. There are four randomized trials of antihypertensive treatment after stroke indicating a tendency of reduced risk of stroke recurrence. Three studies of antihypertensive treatment after first stroke are in progress. Prevention of recurrent stroke is well documented in atrial fibrillation where warfarin is highly beneficial and aspirin has some effect. Carotid endarterectomy in high grade carotid artery stenosis is also well documented. Antiplatelet therapy provides secondary prevention in most types of ischemic brain disease.

Carotid Stenosis↗
PubMed2000

Acute neurological stroke care in Europe: results of the European Stroke Care Inventory.

Following the 1997 Recommendations of the EFNS Task Force on Acute Neurological Stroke Care (European Journal of Neurology, 1997: 4:435-441) a European Inventory was undertaken to assess the development of acute stroke care in the EFNS member countries and to give an estimate of the needs based on 1997 data. All 30 members of the EFNS Stroke Scientist Panel were asked to complete a questionnaire on acute stroke epidemiology as well as acute stroke care in their country. Data were based either on national surveys, hospital statistics, or estimates given on the basis of extrapolation of regional studies, or other defined sources. Specialist estimates were also taken into account where no other data source was available. Data from 22 countries were received and referred to almost one million strokes occurring per year in a population of over 500 million. Most epidemiological data confirmed an east-west gap known from previous studies. These included rates that, in eastern countries, were higher for incidence, stroke as a leading cause of death, and 30-day case-fatality, and rates that were lower for overall hospitalization or availability of CT scanning. East-west differences were not seen for the total number of acute stroke units or the number of acute stroke units set up within neurological hospital departments, nor for most other quality indicators of acute stroke care with the exception of technological standards in some countries. The higher rates for 30-day case-fatality in eastern Europe (mostly above 20%) compared with western Europe (mostly below 20%) are probably caused by a case mix with more severe ischemic strokes and a higher percentage of cerebral haemorrhages admitted for acute care in eastern Europe. This is probably due to the higher prevalence of the most common risk factors for stroke in these countries which tend to result in more severe strokes. This, therefore, underlines the need for stroke prevention programmes especially in eastern Europe. This epidemiological east-west gap is not reflected by most quality indicators for acute stroke care, e.g. total number of acute stroke units available within each country. Most eastern European countries have a well-developed neurological care system for acute stroke but still have urgent technological and socioeconomical needs. The leading role of clinical neurology in acute stroke care is visible in most but not all European countries.

Aged↗
PubMed2000

Danish type gelsolin related amyloidosis: 654G-T mutation is associated with a disease pathogenetically and clinically similar to that caused by the 654G-A mutation (familial amyloidosis of the Finnish type).

BACKGROUND: Familial amyloidosis of the Finnish type (FAF, Finnish hereditary amyloidosis) is caused by a 654G-A mutation in the gelsolin gene on chromosome 9 resulting in the expression of mutant Asn-187 gelsolin which is abnormally proteolytically processed generating amyloidogenic fragments that polymerize into amyloid fibrils. We have recently shown that in a Danish and a Czech family with a clinical syndrome similar to FAF, including corneal lattice dystrophy, cranial neuropathy and skin changes, the disease is caused by another mutation at the same position, namely 654G-T predicting a Try-for-Asp substitution at 187 in secreted gelsolin. AIM: To undertake a closer examination of the Danish subtype of FAF and report immunohistochemical and biochemical findings. RESULTS: Immunostaining of plasma gelsolin isolated from heterozygous FAF of the Danish subtype revealed a pattern similar to that found in FAF-Asn 187. The > 60 kDa gelsolin species contain an epitope characteristic of the amyloid forming region as revealed by an amyloid specific antibody, whereas the approximately 50 kDa fragments are devoid of it. Compared with the wild-type gelsolin peptide (Asp-187), the corresponding mutant peptide (Tyr-187) showed dramatically increased fibrillogenicity as revealed by quantitative thioflavine-T based fluorimetry; ultrastructurally, amyloid-like fibrils were formed by the mutant peptide. Immunohistochemistry showed that antibodies directed against residues 231-242 of secreted gelsolin, representing the carboxy terminus of the sequence forming the amyloid protein (residues 173-243) laid down in the tissues in a fibrillar form in FAF, specifically labelled the amyloid deposited in rectum and skin in the Danish (654G-T) subtype. CONCLUSIONS: The 654G-T mutation in the gelsolin gene gives rise to an amyloid disease clinically and pathogenetically similar to that caused by the 654G-A mutation.

Amyloid↗
PubMed1999

[Direct costs of transient cerebral ischemia. A hospital-based study of resource use in Denmark during the first year following transient cerebral ischemic attack].

In order to obtain knowledge of costs of health care and social services for patients who have transient ischaemic attacks (TIA) all patients admitted to a university hospital in Copenhagen, Denmark, with TIA during 12 months in 1994-1995 were included in a database. The patients were followed until one year after admission and data on resource use during and after the hospital stay were collected prospectively at interviews. The cost of the hospital stay had a mean of 10,100 DKK (1,800 US$) and the cost of health care and social services after discharge had a mean of 8,800 DKK (1,600 US$) per person.

Adult↗