Sensory stimulation in acute stroke therapy

Abstract

The beneficial effects of cortical activation for functional recovery after ischemic stroke have been well described. However, little is known about the role of early sensory stimulation, i.e. stimulation during first 6 h after stroke onset even during acute treatment. In recent years, various preclinical studies reported significant effects of acute sensory stimulation that range from entire neuroprotection to increased infarct volumes by 30-50%. Systematic knowledge about the effect of acute sensory stimulation on stroke outcome is highly relevant as stroke patients are subject to uncontrolled sensory stimulation during transport, acute treatment, and critical care. This article discusses the current stage of knowledge about acute sensory stimulation and provides directions for future experimental and clinical trials.

Keywords: Collateral reperfusion; cortical activation; ischemic stroke; sensory stimulation; stroke models.

Figure 1.

The role of sensory stimulation during the acute phase of ischemic stroke. The cerebral blood flow threshold for neuronal activation increases with time elapsed after arterial occlusion. Therefore, early sensory stimulation is more likely to activate viable cortical areas than delayed stimulation, e.g. 3 h after stroke onset (blue box). Cortical activation increases the regional oxygen demand and might lead to supply–demand mismatch in case of insufficient collateral flow. Supply–demand mismatch transients may in turn trigger peri-infarct depolarizations that worsen stroke outcome (red box). Conversely, cortical activation induced by early stimulation leads to neurovascular coupling that enhances collateral flow through an efficient system of cerebral anastomoses. Enhanced collateral flow is the supposed mechanism that mediates reperfusion and improves clinical outcome in the concept of early sensory stimulation-induced neuroprotection (green box).