Cerebrovascular diseases
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Busy strokologists often find little time for scientific writing. They sometimes develop a mental condition equivalent to that known by neurologists as writer's cramp. It may result in permanent damage to academic career. This paper provides advice how to prevent or treat this condition. ⋯ Conclusions have to be based on the present study findings. The time of lengthy and unfounded speculations is over. A simple message in a clearly written manuscript will get noticed and may advance our understanding of stroke.
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Cerebrovascular diseases · Jan 2004
ReviewOrganization of medical care in acute stroke: importance of a good network.
Stroke is a medical emergency which requires hospital care. Therapeutic and effective organizative measures, such as thrombolysis and stroke units, are available, but early attention is required, as the benefits are time dependent (therapeutic window). ⋯ The main points are reviewed: delay in attention, knowledge and attitude towards stroke, emergency transportation, neurological attention, educational campaigns, clinical protocols and pathways, stroke codes, and existing resources for care. The organization must be modified to have the resources for care necessary for attending acute stroke available, if we want to achieve the real objective of maximum benefit for our patients as set out in the Declaration of Helsingborg.
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Cerebrovascular diseases · Jan 2004
International carotid stenting study: protocol for a randomised clinical trial comparing carotid stenting with endarterectomy in symptomatic carotid artery stenosis.
Carotid stenting avoids general anaesthesia, cranial nerve injury and the discomforts of surgical treatment of carotid stenosis. A systematic review of the randomised trials showed no overall difference in the major risks of endovascular treatment for carotid stenosis compared with surgery, but the confidence intervals were wide and both methods carried a significant risk of stroke. The use of protection devices appears to improve the safety of endovascular treatment, but there are little randomised data available about long-term outcomes. We have therefore set up an international, multicentre, randomised, controlled, open, prospective clinical trial, namely the International Carotid Stenting Study (ICSS), also known as CAVATAS-2. The objectives of the ICSS are to compare the risks, benefits and cost-effectiveness of a treatment policy of referral for carotid stenting compared with referral for carotid endarterectomy. ⋯ The ICSS protocol incorporates a number of novel features to ensure patient safety, including the concept of probationary centres, proctoring of inexperienced investigators and monitoring of individual centre results on an ongoing basis. The protocol is also designed to mirror routine clinical practice as far as possible, so that the results will be widely applicable and relevant to determining the place of carotid stenting in clinical practice in the future.
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Cerebrovascular diseases · Jan 2004
ReviewNeuroprotection in cerebral ischaemia: facts and fancies--the need for new approaches.
'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. ⋯ 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. FANCIES: 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. WHY HAVE NEUROPROTECTIVE AGENTS FAILED IN HUMAN STROKE TRIALS? 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. WHAT CAN BE DONE? FUTURE NEW APPROACHES: IN ANIMAL MODELS, 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. IN CLINICAL TRIALS, 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.