Predictors of deteriorating cerebral infarct: role of inflammatory mechanisms

The development of neurological deterioration in the hours following the stroke onset occurs in somewhat more than 1 in 3 cerebral infarcts and is associated with an increase in morbidity and mortality. This early deterioration (0--48/72 h) entails the conversion of the ischemic penumbra area in an irreversible lesion, a process that is mediated as much by hemodynamic changes in the local cerebral circulation as by biochemical mechanisms. Late neurological deterioration (3--7 days) is more frequently associated with systemic causes. Knowledge of the various clinical, biochemical and imaging markers associated with neurological deterioration is consequently of fundamental importance. For their repercussion in clinical practice, we classify these predictors of deteriorating cerebral infarct into nonmodifiable, modifiable and possibly modifiable. The reduction in cerebral blood flow in a particular cerebral zone causes very early cerebral damage as a consequence of a significant liberation of neuroexcitatory amino acids, followed by an excessive entry of calcium into the interior of cells; this process causes lipid peroxidation, disintegration of the cellular membranes, nuclear destruction and neuronal death. Moreover, ischemia and posterior reperfusion induce an inflammatory response leading to further cellular destruction. It is therefore conceivable that therapeutic interventions aimed at decreasing proinflammatory cytokines and cell adhesion molecules might result in better outcome in this population.