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Review
. 2023 Sep 23;11(10):2617.
doi: 10.3390/biomedicines11102617.

Integrative Approaches in Acute Ischemic Stroke: From Symptom Recognition to Future Innovations

Affiliations
Review

Integrative Approaches in Acute Ischemic Stroke: From Symptom Recognition to Future Innovations

Vicentiu Mircea Saceleanu et al. Biomedicines. .

Abstract

Among the high prevalence of cerebrovascular diseases nowadays, acute ischemic stroke stands out, representing a significant worldwide health issue with important socio-economic implications. Prompt diagnosis and intervention are important milestones for the management of this multifaceted pathology, making understanding the various stroke-onset symptoms crucial. A key role in acute ischemic stroke management is emphasizing the essential role of a multi-disciplinary team, therefore, increasing the efficiency of recognition and treatment. Neuroimaging and neuroradiology have evolved dramatically over the years, with multiple approaches that provide a higher understanding of the morphological aspects as well as timely recognition of cerebral artery occlusions for effective therapy planning. Regarding the treatment matter, the pharmacological approach, particularly fibrinolytic therapy, has its merits and challenges. Endovascular thrombectomy, a game-changer in stroke management, has witnessed significant advances, with technologies like stent retrievers and aspiration catheters playing pivotal roles. For select patients, combining pharmacological and endovascular strategies offers evidence-backed benefits. The aim of our comprehensive study on acute ischemic stroke is to efficiently compare the current therapies, recognize novel possibilities from the literature, and describe the state of the art in the interdisciplinary approach to acute ischemic stroke. As we aspire for holistic patient management, the emphasis is not just on medical intervention but also on physical therapy, mental health, and community engagement. The future holds promising innovations, with artificial intelligence poised to reshape stroke diagnostics and treatments. Bridging the gap between groundbreaking research and clinical practice remains a challenge, urging continuous collaboration and research.

Keywords: acute ischemic stroke; cerebrovascular disease; endovascular thrombectomy; fibrinolytic therapy; neuroimaging; neuroradiology; neurovascular treatment; revascularization; stroke onset symptoms.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Illustrative Overview of Blood–Brain Barrier Dynamics in the Wake of Acute Ischemic Stroke.
Figure 2
Figure 2
The intricate processes leading to ischemic neuronal cell death involve various molecular pathways and interactions. When NMDA receptors (NMDARs) and AMPA receptors (AMPARs) are stimulated, there is an elevation in the levels of calcium within the cell’s cytoplasm. This heightened calcium concentration triggers the activation of enzymes known as calpains and induces dysfunction within the mitochondria. Simultaneously, the binding of Fas ligands (FasL) to their counterparts, the Fas death receptors, sets off the activation of a protein called caspase 8. These activated calpains, together with caspase 8, collaborate to cleave a protein named Bid, transforming it into its truncated version, tBid. Once formed, tBid associates with another protein, Bax, on the mitochondrial membrane. This interaction is critical as it results in the creation of pores in the membrane, leading to the expulsion of several vital molecules: cytochrome c (Cyt c), apoptosis-inducing factor (AIF), and the harmful reactive oxygen species (ROS). After their release, both ROS and AIF relocate to the cell’s nucleus. Here, they play a pivotal role in damaging the DNA and initiating specific neuronal cell death pathways. A prime example of such a pathway is the phosphorylation of the protein p53, which, when phosphorylated (Pp53), activates the MAPK signaling route, pushing the cell towards apoptosis. Additionally, the expelled cytochrome c from the mitochondria plays a role outside its traditional function. In the cell’s cytoplasm, cytochrome c collaborates with the apoptotic protein activating factor-1 (APAF-1) and procaspase 9 to assemble into a complex known as the apoptosome. This structure is integral to the internal apoptotic pathway, further cementing the neuron’s fate towards programmed cell death.
Figure 3
Figure 3
Comparison of Traditional Stroke Prognostic Management vs. Enhanced Approach Using Point-of-Care-Tests (POCTs).

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