Abstract:BACKGROUND AND PURPOSE
The presence of collaterals is associated with a reduced risk of stroke and transient ischemic attack (TIA) in patients with steno-occlusive carotid artery disease. Although metabolic syndrome negatively impacts collateral status, it is unclear whether and to what extent type 2 diabetes (T2DM) affects cerebral collateral flow regulation during hypoperfusion.
METHODS
We examined the spatial and temporal changes of the leptomeningeal collateral flow and the flow dynamics of the penetrati… Show more
“…We found that the delta power was only transiently increased for less than 5 min in the hippocampal slm layer following an episode of mild ischemia via bilateral CCAO; interestingly, it normalized quickly likely due to the robust collateral flow compensation via the circle of Willis. 58 Similar changes in delta power were detected in the contralateral hippocampus (Figure 4). Figure 4.Cortical stroke induces temporary reduction in the power of theta and gamma oscillation in the hippocampal slm.…”
The functional consequences of ischemic stroke in the remote brain regions are not well characterized. The current study sought to determine changes in hippocampal oscillatory activity that may underlie the cognitive impairment observed following distal middle cerebral artery occlusion (dMCAO) without causing hippocampal structural damage. Local field potentials were recorded from the dorsal hippocampus and cortex in urethane-anesthetized rats with multichannel silicon probes during dMCAO and reperfusion, or mild ischemia induced by bilateral common carotid artery occlusion (CCAO). Bilateral change of brain state was evidenced by reduced theta/delta amplitude ratio and shortened high theta duration following acute dMCAO but not CCAO. An aberrant increase in the occurrence of sharp-wave-associated ripples (150â250âHz), crucial for memory consolidation, was only detected after dMCAO reperfusion, coinciding with an increased occurrence of high-frequency discharges (250â450âHz). dMCAO also significantly affected the modulation of gamma amplitude in the cortex coupled to hippocampal theta phase, although both hippocampal theta and gamma power were temporarily decreased during dMCAO. Our results suggest that MCAO may disrupt the balance between excitatory and inhibitory circuits in the hippocampus and alter the function of cortico-hippocampal network, providing a novel insight in how cortical stroke affects function in remote brain regions.
“…We found that the delta power was only transiently increased for less than 5 min in the hippocampal slm layer following an episode of mild ischemia via bilateral CCAO; interestingly, it normalized quickly likely due to the robust collateral flow compensation via the circle of Willis. 58 Similar changes in delta power were detected in the contralateral hippocampus (Figure 4). Figure 4.Cortical stroke induces temporary reduction in the power of theta and gamma oscillation in the hippocampal slm.…”
The functional consequences of ischemic stroke in the remote brain regions are not well characterized. The current study sought to determine changes in hippocampal oscillatory activity that may underlie the cognitive impairment observed following distal middle cerebral artery occlusion (dMCAO) without causing hippocampal structural damage. Local field potentials were recorded from the dorsal hippocampus and cortex in urethane-anesthetized rats with multichannel silicon probes during dMCAO and reperfusion, or mild ischemia induced by bilateral common carotid artery occlusion (CCAO). Bilateral change of brain state was evidenced by reduced theta/delta amplitude ratio and shortened high theta duration following acute dMCAO but not CCAO. An aberrant increase in the occurrence of sharp-wave-associated ripples (150â250âHz), crucial for memory consolidation, was only detected after dMCAO reperfusion, coinciding with an increased occurrence of high-frequency discharges (250â450âHz). dMCAO also significantly affected the modulation of gamma amplitude in the cortex coupled to hippocampal theta phase, although both hippocampal theta and gamma power were temporarily decreased during dMCAO. Our results suggest that MCAO may disrupt the balance between excitatory and inhibitory circuits in the hippocampus and alter the function of cortico-hippocampal network, providing a novel insight in how cortical stroke affects function in remote brain regions.
“…It can accurately determine the degree of carotid artery stenosis and is easy to operate, inexpensive, reproducible, safe, and intuitive. Therefore, it is still the test of choice to diagnose and screen carotid artery diseases [23,24]. Our results showed that the AUC predicted by the TSS values calculated on ultrasonography were > 0.7 for all prognostic end points, and no significant differences in AUC was found between ultrasonographic prediction and CTA, MRA, or GBF (all P > 0.05).…”
Introduction To improve the accuracy of ultrasound techniques for the assessment of carotid stenosis, we designed a novel carotid artery stenosis ultrasound scale (CASUS), and evaluated its accuracy, reliability, and its value in predicting the occurrence of cardiovascular and cerebrovascular diseases in a prospective study. Methods A total of 750 patients with first-time ischemic stroke and hospitalized within 24 h were enrolled in the study. Using color Doppler ultrasound (CDUS), the degree of stenosis and blood flow (BF) in bilateral internal carotid arteries (ICA) and the V1-V3 segment of vertebral arteries (VA) was assessed. Cubic simulation curves for BF and global blood flow (GBF) over the stenosis score (SS), total stenosis score (TSS), and radiological imaging-total stenosis score (RI-TSS) were fitted and compared. The receiver operating characteristic (ROC) curves using TSS, RI-TSS, or GBF to predict various ischemic stroke endpoints were also analyzed and compared. Results There was a linear relationship between SS and BF both ICA and VA (R2 were 0.734 and 0.783, respectively, both P < 0.05). Both TSS and RI-TSS with GBF showed an inverse "S" curve relationship (R2 was 0.839 and 0.843, all P < 0.05). The AUC values of TSS-based and RI-TSS-based predictions of each endpoint were all greater than 0.7 (all P < 0.05), but the differences of the AUC values between TSS, RI-TSS, and GBF were not statistically significant (all P > 0.05). Conclusions The novel CASUS can better reflect the level of cerebral reperfusion in patients with ischemic stroke and can better predict the occurrence of cardiovascular and cerebrovascular diseases. Keywords Brain ischemic. Carotid stenosis. Ultrasound. Neuroimaging. Cerebral blood flow Yi Tang and Ming-yu Wang contributed equally to this work.
“…Evidence from animal experiments and clinical trials has suggested that the early and marked CBF restoration in ischemic brain plays a critical role in tissue repair and functional recovery after ischemic injury (Li et al, 2007; El Amki and Wegener, 2017). Accumulating evidence has shown that adaptive responses in the brain following CCH include angiogenesis and dilation of collateral vessels for CBF restoration (Jing et al, 2015; Nishijima et al, 2016; Xiong et al, 2017). In this study, we found that astrocyte activation, neuronal loss and apoptosis may also contribute to cognitive impairment in CCH rats.…”
Compensatory vascular mechanisms can restore cerebral blood flow (CBF) but fail to protect against chronic cerebral hypoperfusion (CCH)-mediated neuronal damage and cognitive impairment. Prostaglandin E1 (PGE1) is known as a vasodilator to protect against ischemic injury in animal models, but its protective role in CCH remains unclear. To determine the effect of PGE1 on cerebral hemodynamics and cognitive functions in CCH, bilateral common carotid artery occlusion (BCCAO) was used to mimic CCH in rats, which were subsequently intravenously injected with PGE1 daily for 2 weeks. Magnetic resonance imaging, immunofluorescence staining and Morris water maze (MWM) were used to evaluate CBF, angiogenesis, and cognitive functions, respectively. We found that PGE1 treatment significantly restored CBF by enhancing vertebral artery dilation. In addition, PGE1 treatment increased the number of microvascular endothelial cells and neuronal cells in the hippocampus, and decreased the numbers of astrocyte and apoptotic cells. In the MWM test, we further showed that the escape latency of CCH rats was significantly reduced after PGE1 treatment. Our results suggest that PGE1 ameliorates cognitive dysfunction in CCH rats by enhancing CBF recovery, sustaining angiogenesis, and reducing astrocyte activation and neuronal loss.
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