| 1. |
- Ahmed, N, et al.
(författare)
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Effects of blood pressure lowering in the acute phase of total anterior circulation infarcts and other stroke subtypes
- 2003
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Ingår i: Cerebrovascular diseases (Basel, Switzerland). - : S. Karger AG. - 1015-9770 .- 1421-9786. ; 15:4, s. 235-243
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Tidskriftsartikel (refereegranskat)abstract
- <i>Background:</i> Lowering of blood pressure (BP) in the acute phase of stroke is reported both to worsen and to improve the outcome. To investigate whether heterogeneity exists between stroke subtypes in the response to BP lowering, we analysed data from the Intravenous Nimodipine West European Stroke Trial (INWEST). <i>Methods:</i> INWEST enrolled acute ischaemic stroke patients within 24 h (n = 295) to the following groups: placebo (n = 100), 1 mg/h nimodipine (n = 101) or 2 mg/h nimodipine (n = 94). Patients were retrospectively classified as total anterior circulation infarct (TACI) (i.e. hemiparesis + hemianopia + dysphasia) and non-TACI (exclusion of any one of these). Main outcome measures were neurological (Orgogozo) and functional (Barthel) scores at day 21. <i>Results:</i> 106 patients were labelled as TACI and 62 as non-TACI. No significant difference in BP was observed between the TACI and non-TACI subtypes at baseline, nor did the subtypes differ in BP course within the treatment groups. A higher proportion of non-TACI patients received postrandomisation antihypertensive agents in addition to the study drug compared with TACI patients (55% non-TACI vs. 26% TACI, p < 0.005). For TACI patients, there was no outcome difference between the placebo- and nimodipine-treated groups. For non-TACI patients, placebo had a significantly better neurological (p = 0.004) and functional (p = 0.04) outcome than the high-dose nimodipine group. In multivariate analysis for TACI patients, BP reduction and nimodipine treatment had no relation with outcome. Baseline stroke severity (p < 0.005) was the only significant predictor of the outcome at day 21. For non-TACI patients, diastolic BP (DBP) reduction (p = 0.03) and nimodipine treatment (p = 0.001) were related to neurological deterioration and nimodipine treatment (p = 0.01) to functional deterioration. Systolic BP reduction was associated with neurological (p < 0.005) and functional improvement (p = 0.01). Baseline stroke severity (p < 0.005) was related to both neurological and functional outcome. <i>Conclusion:</i> BP lowering and nimodipine treatment had no significant effect on outcome for TACI patients. For non-TACI patients, DBP lowering worsened the neurological outcome and high-dose nimodipine worsened both the neurological and functional outcome.
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| 2. |
- Ahmed, N, et al.
(författare)
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Salivary cortisol, a biological marker of stress, is positively associated with 24-hour systolic blood pressure in patients with acute ischaemic stroke
- 2004
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Ingår i: Cerebrovascular diseases (Basel, Switzerland). - : S. Karger AG. - 1015-9770 .- 1421-9786. ; 18:3, s. 206-213
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Tidskriftsartikel (refereegranskat)abstract
- <i>Background/Aim:</i> The cause of elevated blood pressure (BP) in acute stroke is unknown. Stress is often suggested as a main contributing factor. We aimed to investigate the relationship between BP and stress in patients with acute stroke. <i>Methods:</i> 58 patients with clinical symptoms of stroke were recruited prospectively after exclusion of haemorrhage by CT scan within 14 h and 15 min (mean) after symptom onset (range 2 h and 45 min–23 h and 40 min). The mean age of the patients was 66 years (range 39–86 years), and the mean National Institute of Health Stroke Scale score was 7 (range 1–26). BP and pulse rate were recorded by non-invasive automatic monitoring hourly for 24 h. Stress was evaluated by testing the level of salivary cortisol. Four samples of saliva were obtained at inclusion, on the evening of the inclusion day (20.00–22.00 h), on the morning of the next day (7.00–9.00 h) and on the afternoon of the inclusion day/next day (15.00–17.00 h) within 24 h after inclusion in the study. Logarithmic transformation was done for cortisol levels. <i>Results:</i> The 24-hour mean cortisol level (geometric mean 13.6 nmol/l) was related to 24-hour mean systolic BP [SBP; r = 0.36, p = 0.01, multivariate p = 0.02], mean night-time (22.00–6.00 h) SBP (r = 0.43, p = 0.001, multivariate p < 0.005) and mean night-time diastolic BP (r = 0.31, p = 0.02, multivariate p = 0.02). Cortisol levels at inclusion (r = 0.31, p = 0.02, multivariate p = 0.05 for 24-hour SBP) and in the evening were also statistically significantly related to the above BP variables. The morning cortisol (r = 0.28, p = 0.04, multivariate p = 0.04) was related to night-time SBP. <i>Conclusions:</i> Salivary cortisol was positively correlated with 24-hour SBP and night-time BP, suggesting that stress is a contributing factor for high BP in acute stroke.
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| 3. |
- Martinsson, L, et al.
(författare)
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Intensive early physiotherapy combined with dexamphetamine treatment in severe stroke: a randomized, controlled pilot study
- 2003
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Ingår i: Cerebrovascular diseases (Basel, Switzerland). - : S. Karger AG. - 1015-9770 .- 1421-9786. ; 16:4, s. 338-345
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Tidskriftsartikel (refereegranskat)abstract
- <i>Background:</i> The most severely disabled stroke patients are often excluded from studies evaluating effects of physiotherapy. This study intended to investigate the effect of an increased intensity of physiotherapy in combination with dexamphetamine the first week after ischemic stroke in patients with an impaired level of consciousness and severe motor dysfunction. <i>Methods:</i> Thirty patients were enrolled within 96 h after onset of symptoms. Patients were randomized to 30–45 min of physiotherapy twice daily or to maximally 15 min per day for 5 days. All patients received dexamphetamine to achieve alertness. Functional outcome measures were assessed at baseline, the day after treatment discontinuation, and 3 and 12 months after stroke onset. Residence of living was registered at long-term follow-ups. <i>Results:</i> No statistically significant differences were seen between groups in the outcomes measured at any time point. However, both groups improved over time in all outcomes at 3 and 12 months (p < 0.05), except for sensory functions at 3 months and motor functions at 12 months. The number of patients needed to treat (NNT) to achieve the desired improvement in Lindmark motor score was 8, with the 95% CI being NNT(harm) 10 to NNT(beneficial) 3. The fraction of patients who died was the same in both treatment groups, 47% (95% CI 28–65%). <i>Conclusions:</i> An increased intensity of physiotherapy in combination with dexamphetamine during the first week after stroke onset did not affect short- or long-term outcome in this limited sample of patients with severe stroke.
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| 4. |
- Ringleb, PA, et al.
(författare)
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Guidelines for management of ischaemic stroke and transient ischaemic attack 2008
- 2008
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Ingår i: Cerebrovascular diseases (Basel, Switzerland). - : S. Karger AG. - 1421-9786 .- 1015-9770. ; 25:5, s. 457-507
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Tidskriftsartikel (refereegranskat)abstract
- This article represents the update of the European Stroke Initiative Recommendations for Stroke Management. These guidelines cover both ischaemic stroke and transient ischaemic attacks, which are now considered to be a single entity. The article covers referral and emergency management, Stroke Unit service, diagnostics, primary and secondary prevention, general stroke treatment, specific treatment including acute management, management of complications, and rehabilitation.
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| 5. |
- Wahlgren, NG, et al.
(författare)
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Neuroprotection in cerebral ischaemia: facts and fancies--the need for new approaches
- 2004
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Ingår i: Cerebrovascular diseases (Basel, Switzerland). - : S. Karger AG. - 1015-9770 .- 1421-9786. ; 1717 Suppl 1, s. 153-166
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Tidskriftsartikel (refereegranskat)abstract
- ‘Neuroprotection’ is a term used to describe the putative effect of interventions protecting the brain from pathological damage. In occlusive stroke, the concept of neuroprotection involves inhibition of a cascade of pathological molecular events occurring under ischaemia and leading to calcium influx, activation of free radical reactions and cell death. This article will summarize neuroprotection trials to date, some facts and fancies about neuroprotection, ischaemic pathophysiology and possible reasons for the apparent failure of human neuroprotective stroke trials. <i>Facts: </i>In the acute stage of occlusive stroke, moderate reduction of blood flow results in a ‘penumbra’ of brain cells, often surrounding a core infarct, in which brain cells survive for a few hours but gradually die if reperfusion is not established. Increased knowledge of the complex pathophysiology in acute ischaemic stroke has led to the development of a great number of candidates for neuroprotective interventions. Many neuroprotective agents have proven efficacious in animal models, but so far no human study has shown a statistically significant benefit in patients with acute ischaemic stroke on primary endpoint measures. Some neuroprotective agents show beneficial effects on post hoc analyses, and some studies are still ongoing. <i>Fancies: </i>In the early years of neuroprotective studies in stroke, it was thought that a drug with almost no adverse effects could be given by ambulance staff on the way to hospital and induce a clinically significant effect on outcome. Since there were only benefits and no risks, diagnostic skills by neurologists and neuroradiological evaluations would no longer be required. <i>Why Have Neuroprotective Agents Failed in Human Stroke Trials? </i>There are several possible explanations why neuroprotective trials have been unable to prove an effect in addition to the eventuality that the basic concept is wrong. The effects of neuroprotective agents on infarct size are time dependent, and treatment has often been initiated much later than in successful experimental stroke models. Insufficient doses of the drugs and slow availability of the drug at the target area may be other explanations. Too small sample sizes in trials and imbalance of prognostically important baseline variables are examples of shortcomings in trial methodology. <i>What Can Be Done? Future New Approaches: </i><i>In animal models,</i> preclinical testing of neuroprotective candidates should be standardized. Conventional stroke models with young and healthy animals may be replaced by older animals with common co-morbidity such as atherosclerosis. Highly effective new neuroprotective agents need to be discovered, and combination therapies should be tried. <i>In clinical trials,</i> the greatest chances of success may be with neuroprotective concepts involving mechanisms in both ischaemic and reperfusion pathophysiology, in combination with a thrombolytic therapy protocol. Neuroprotective agents, possibly combinations of agents, should preferably approach several of these mechanisms. Treatments should be initiated early, at least within 3 h after stroke onset, by an intravenous route. The selected compound(s) should easily pass the blood-brain barrier. Neuroprotective agents shown to be highly effective in stroke models should be preferred, and doses used experimentally should be used also in the clinical setting. Trials should use randomization techniques, which reduce imbalances of prognostically important baseline variables, and the estimated sample size of a trial should be based on expectations of a modest clinical effect.
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