Plasmatic markers for early diagnostic and treatment decisions in ischemic stroke.

A neurologic deficit of sudden onset conforming to a vascular territory is a clear clinical indication that a patient suffers from an acute stroke. However, the imagistic diagnostic confirmation is not always readily available. We are now able to offer comprehensive medical support for the patient after an acute stroke and to make a prodigious rehabilitation program after the damage is done, but this is not offering the chance for improvement. An opportunity to better diagnose ischemic stroke seems to be available by using neuronal biomarkers. Extensive research is being conducted in this field and useful information is beginning to gather. This mini-review aims to highlight selected studies that appear to be of particular interest for the clinical neurologist. The most promising biomarkers (or rather panels of biomarkers) are presented with theirs clinical usefulness and limitations.

Plasmatic markers in hemorrhagic stroke.

Stroke is the third most common cause of death in the United States and it is the leading cause of disability. Early diagnosis and immediate therapeutic interventions are important factors to reduce the extent of brain tissue damage and the risk of stroke-related death. A rapid blood test that can confirm the clinical or imaging diagnosis or that can add to the stratification of the risk would be very useful. Such a test has to be validated in large studies and has to be based on a simple and low-cost technology. Many biological markers were tested for their ability to serve as 'would-be' stroke biological markers; some of them appear to have a place in the diagnostic work-up of stroke patients. These molecules include Glial Fibrillary Acidic Protein (GFAP), the N-methyl-D-aspartate receptor (NMDA), APO C-III, APO C-I, PARK7, nucleoside diphosphate kinase A (NDKA), S100B, B-type neurotrophic growth factor, von Willebrand factor, matrix metalloproteinase-9, and monocyte chemotactic protein-1. There are obvious limitations to this study, among them the fact that disability does not necessarily correlate with the amount of cerebral tissue lost (the site of stroke may be more important) and the role of the blood-brain barrier in delaying the release of the neuronal proteins in the blood stream. Further studies are awaited to confirm the role of these molecules in the management of acute stroke patients.