ArticleQuantitative imaging in medicine and surgery2021
Quantitative research on the interaction between cerebral edema and peripheral cerebral blood perfusion using swept-source optical coherence tomography.
Article in Quantitative imaging in medicine and surgery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors at 2 institutions in 2 countries.
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Abstract
backgroundIschemic cerebral edema (CE) is a major leading cause of death in patients with ischemic stroke. The CE progression is closely related to the local cerebral blood perfusion (LCBP) level surrounding the edema area. Quantitative studying the interaction between the CE and peripheral LCBP may provide new inspiration for control and even treatment of CE.
methodsPhotothrombosis ischemia mouse model was established and observed for 9 hours using swept-source optical coherence tomography (SS-OCT). OCT-based angiography and OCT-based attenuation imaging techniques were used to reconstruct the angiograms reflecting the cerebral blood perfusion (CBP) level and optical attenuation coefficient (OAC) maps reflecting the edema state. The influence of edema on LCBP was analyzed by quantifying the blood perfusion in different spatial locations around the edema tissue, and the influence of LCBP on CE progression was revealed by comparing the changes of the edema area and LCBP level over time.
resultsPreliminary studies show that the effect of edema tissue on LCBP is very significant, which shows a clear spatial dependence. LCBP near the edema tissue is 15-20% lower than that far away from the edema tissue. When the LCBP drops to around 60% of the initial value, the edema area increases sharply. In addition, the level of CBP in the contralateral hemisphere also decreases with time. When the contralateral CBP drops to around 60%, there is a certain probability that contralateral edema will occur.
conclusionsCE progression is not only related to the LCBP around the edema tissue but also related to the CBP of non-edematous regions. Controlling the CBP level of non-edematous regions may play a positive role in the treatment of CE. This work provides a new method and inspiration for exploring the mechanism of ischemic CE progression.
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