Neuroprotection in Acute Ischemic Stroke: A Battle Against the Biology of Nature

Abstract

Stroke is the second most common cause of global death following coronary artery disease. Time is crucial in managing stroke to reduce the rapidly progressing insult of the ischemic penumbra and the serious neurologic deficits that might follow it. Strokes are mainly either hemorrhagic or ischemic, with ischemic being the most common of all types of strokes. Thrombolytic therapy with recombinant tissue plasminogen activator and endovascular thrombectomy are the main types of management of acute ischemic stroke (AIS). In addition, there is a vital need for neuroprotection in the setting of AIS. Neuroprotective agents are important to investigate as they may reduce mortality, lessen disability, and improve quality of life after AIS. In our review, we will discuss the main types of management and the different modalities of neuroprotection, their mechanisms of action, and evidence of their effectiveness after ischemic stroke.

Etiologies, Evaluation, and Differential Diagnosis of Dysphonia

“…This approach can be remarkably useful in the evaluation process since some details cannot be obtained by rigid or flexible endoscopic approaches. Stroboscopy-based surveillance might also be useful in evaluating patients suffering from related malignancies (21,22).…”

Neuroprotection in Stroke

“…As stroke is still second cause of death and disability in the world, in spite of the clear improvement of treatment modalities, additional treatment strategies for this condition remain challenging [1]. Neuroprotection as an add-on therapy in stroke is a promising idea, and the number of studies investigating possible neuroprotective agents or methods is rising [2]. Due to variety of the neuronal death mechanisms following the disruption of the blood supply, the possible therapeutic approaches should vary as well.…”

“…Due to variety of the neuronal death mechanisms following the disruption of the blood supply, the possible therapeutic approaches should vary as well. Most important mechanisms of brain tissue damage are neuronal excitotoxicity, periinfarct depolarizations, local and distant inflammation, cellular apoptosis, and oxidative stress [2][3][4][5]. Furthermore, it is proven that free radical oxygen species (ROS) as well as calcium play an important role in increasing the inflammatory response by raising the levels of inflammatory cytokines and endothelial cell-adhesion molecules [2,3,6,7].…”

“…Most important mechanisms of brain tissue damage are neuronal excitotoxicity, periinfarct depolarizations, local and distant inflammation, cellular apoptosis, and oxidative stress [2][3][4][5]. Furthermore, it is proven that free radical oxygen species (ROS) as well as calcium play an important role in increasing the inflammatory response by raising the levels of inflammatory cytokines and endothelial cell-adhesion molecules [2,3,6,7]. Development of cerebral edema, a reaction to brain tissue damage, should not be forgotten as an additional factor influencing the final extension of neuronal cell loss as well [8].…”

“…Combining recanalization techniques with neuroprotection remains an attractive idea. Over 1000 neuroprotective agents and methods have been tested in preclinical studies, showing promising results [2,10]. Unfortunately, more than 200 studies involving clinical trials did not provide the same results so far, and only a few have showed some clinical success [2,4,10].…”