Advances in Stroke 2003: Introduction
The generation of new information creates a parallel demand for its analysis, evaluation, and integration with current knowledge. When we introduced Advances in Stroke in the February 2003 issue of Stroke, 9 out of the top 10 accessed articles were from this series. This suggests that the succinct summaries of the most important developments in the previous year fulfilled a need. One remarkable aspect of the series was that it featured some articles co-authored by clinicians and basic scientists in clear language, bridging the common dichotomy between laboratory and clinical approaches.
The year 2003 witnessed the reporting of a strong association between the phosphodiesterase 4D gene and ischemic stroke in Iceland. This sets the stage for the study in other populations and for working out mechanisms. A disease mechanism that is becoming clearer is one explaining the association of hyperhomocysteinemia and stroke. At least part of the answer is that oxidative stress affects the structure and function of the cerebral blood vessels. It turns out that angiotensin II can also harm blood vessels, independently from its role in producing hypertension.
Imaging has unveiled the threat that white matter lesions and silent infarcts pose. Subjects with these changes are twice as likely to develop dementia and 3 times as prone to suffer a stroke than subjects of similar age who do not have them. When a stroke actually occurs, tPA remains the treatment of choice within the first 3 hours but always under the shadow of possible hemorrhage. Experimental data suggest that metalloproteins play a role in this risk of hemorrhage and offer a new potential therapeutic target. Also, preliminary studies promise extension of the 3-hour time window in selected cases through the use of perfusion computerized tomography. Another approach that may improve treatment is the risk classification of acute neurovascular syndromes. When treating acute stroke, hyperglycemia portends risk of a bad outcome and hemorrhage. Now it seems that its treatment may result in better outcomes. Progress is also being made in the treatment of some of the more severe forms of stroke. Although inconclusive, studies support the concept that emergency and intensive care management may have a role in intracerebral hemorrhage and in the malignant middle cerebral artery syndrome.
In prevention, the role of angiotensin-converting enzyme (ACE) inhibitors is gaining new credibility in decreasing stroke risk beyond its effect on hypertension, while in the investigation of carotid disease noninvasive carotid imaging continues to displace angiography as the investigation of choice. Angioplasty and stenting increasingly replace surgery in the management of carotid disease, albeit without the objective evidence to justify this shift in approach.
Another area of progress has been new knowledge about the natural history of unruptured aneurysms and the likely consequences of different treatment choices.
Stroke rehabilitation at last is gaining the role that it deserves. Intensity of therapy, task-specific training, and increased sensory stimulation are finding scientific support for their practice. Vascular cognitive impairment also is getting the recognition and attention that its frequency and importance justify. All the major risk factors for stroke are also risk factors for Alzheimer’s disease, including atrial fibrillation. Ximelagatran now offers an alternative to coumadin for the treatment of patients with atrial fibrillation, while evidence-based clinical practice education provides the rationale not only for treatment but for rehabilitation and prevention. Health policy and outcome research increasingly commands the ear of policy makers, and prevention and health services delivery guide a larger proportion of our efforts.
As always, we welcome comments from our readers and contributors on how to serve them best through this annual series of summarizing articles.