Microemboli as an Etiology of Acute Ischemic Stroke in Watershed zone
Nouran Mohamed Salah El-Dein;
Abstract
Watershed infarct is defined as an ischemia, or blood flow blockage, that is localized to the border zones between the territories of two major arteries in the brain.
Classic neuropathologic studies describe two distinct supratentorial WS areas, one between the cortical territories of the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA), and the other in the white matter along and slightly above the lateral ventricle, between the deep and the superficial arterial systems of the MCA. The former, superficial areas have been commonly referred to as the external watershed (EWS), and the latter have been referred to as the internal watershed (IWS).
Watershed infarcts reportedly account for 10% of all brain infarcts. It has long been debated whether WS infarcts are caused by impaired cerebral perfusion or by embolisms from the heart, aorta, and stenotic parent artery. Many reports have emphasized that WS infarcts are the consequence of hemodynamic compromise (so-called low-flow infarcts), but other reports have suggested that this is not always the case and have insisted that embolization plays a major role in the development of WS infarcts. Some studies have implicated both mechanisms in the pathogenesis of WS infarction; that is, reduced cerebral perfusion may impair the washing out of microemboli, which preferentially involves the border-zone areas.
Whether there are differences in the pathogenesis associated with infarcts within the IWS versus the EWS is unclear, many studies had linked IWS infarcts especially rosary like pattern to hemodynamic compromise, while EWS is related more to microembolism. While other found that EWS could be related to hemodynamic especially if associated with IWS infarcts. Other found that even in IWS and rosary like pattern infarcts, microembolism could have a role in their pathogenesis either alone or combined with hypoperfusion.
The cerebral vasculature has a unique ability to dilate during hypercapnea and to constrict during hypocapnia. These effects of carbon dioxide (CO2) on the cerebral circulation are mostly demonstrated in resistant arterioles and play an important role in cerebral autoregulation that enables constant cerebral blood flow.
Our study represents one of the studies to detect embolic and hemodynamic causes of WSI and correlate between the causes and the site of WSI.
We included 50 patients with acute cerebrovascular ischemic stroke with neuroimaging findings show watershed zone infarction, who admitted to Ain Shams University Hospital within seven days from stroke onset.
Classic neuropathologic studies describe two distinct supratentorial WS areas, one between the cortical territories of the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA), and the other in the white matter along and slightly above the lateral ventricle, between the deep and the superficial arterial systems of the MCA. The former, superficial areas have been commonly referred to as the external watershed (EWS), and the latter have been referred to as the internal watershed (IWS).
Watershed infarcts reportedly account for 10% of all brain infarcts. It has long been debated whether WS infarcts are caused by impaired cerebral perfusion or by embolisms from the heart, aorta, and stenotic parent artery. Many reports have emphasized that WS infarcts are the consequence of hemodynamic compromise (so-called low-flow infarcts), but other reports have suggested that this is not always the case and have insisted that embolization plays a major role in the development of WS infarcts. Some studies have implicated both mechanisms in the pathogenesis of WS infarction; that is, reduced cerebral perfusion may impair the washing out of microemboli, which preferentially involves the border-zone areas.
Whether there are differences in the pathogenesis associated with infarcts within the IWS versus the EWS is unclear, many studies had linked IWS infarcts especially rosary like pattern to hemodynamic compromise, while EWS is related more to microembolism. While other found that EWS could be related to hemodynamic especially if associated with IWS infarcts. Other found that even in IWS and rosary like pattern infarcts, microembolism could have a role in their pathogenesis either alone or combined with hypoperfusion.
The cerebral vasculature has a unique ability to dilate during hypercapnea and to constrict during hypocapnia. These effects of carbon dioxide (CO2) on the cerebral circulation are mostly demonstrated in resistant arterioles and play an important role in cerebral autoregulation that enables constant cerebral blood flow.
Our study represents one of the studies to detect embolic and hemodynamic causes of WSI and correlate between the causes and the site of WSI.
We included 50 patients with acute cerebrovascular ischemic stroke with neuroimaging findings show watershed zone infarction, who admitted to Ain Shams University Hospital within seven days from stroke onset.
Other data
| Title | Microemboli as an Etiology of Acute Ischemic Stroke in Watershed zone | Other Titles | الصمات المتناهية الصغر كمسبب للسكتة الارتوائية في المناطق المستجمعة | Authors | Nouran Mohamed Salah El-Dein | Issue Date | 2016 |
Attached Files
| File | Size | Format | |
|---|---|---|---|
| G13684.pdf | 849.45 kB | Adobe PDF | View/Open |
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